90 results on '"Xian-Yu Liu"'
Search Results
2. Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors
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Devin M. Barry, Xue-Ting Liu, Benlong Liu, Xian-Yu Liu, Fang Gao, Xiansi Zeng, Juan Liu, Qianyi Yang, Steven Wilhelm, Jun Yin, Ailin Tao, and Zhou-Feng Chen
- Subjects
Science - Abstract
The role of gastrin related peptide (GRP+) neurons in itch is debated. Here, the authors generate a conditional knock-in mouse to label and manipulate GRP expressing DRG neurons and investigate their role in itch and nociception.
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- 2020
- Full Text
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3. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk
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Qing-Tao Meng, Xian-Yu Liu, Xue-Ting Liu, Juan Liu, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
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itch ,BNP ,NPRC ,NPRA ,GRP ,spinal cord ,Medicine ,Science ,Biology (General) ,QH301-705.5 - Abstract
Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCβ-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice.
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- 2021
- Full Text
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4. Parametric Modeling Method for 3D Symbols of Fold Structures
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An-Bo Li, Hao Chen, Xiao-Feng Du, Guo-Kai Sun, and Xian-Yu Liu
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fold structure ,3D geological symbols ,parametric modeling ,3D geological modeling ,3D GIS ,visual suggestiveness ,Geography (General) ,G1-922 - Abstract
Most fabrication methods for three-dimensional (3D) geological symbols are limited to two types: directly increasing the dimensionality of a 2D geological symbol or performing appropriate modeling for an actual 3D geological situation. The former can express limited vertical information and only applies to the three-dimensional symbol-making of point mineral symbols, while the latter weakens the difference between 3D symbols and 3D geological models and has several disadvantages, such as high dependence on measured data, redundant 3D symbol information, and low efficiency when displayed in a 3D scene. Generating a 3D geological symbol is represented by the process of constructing a 3D geological model. This study proposes a parametric modeling method for 3D fold symbols according to the complexity and diversity of the fold structures. The method involves: (1) obtaining the location of each cross-section in the symbol model, based on the location parameters; (2) constructing the middle cross-section, based on morphological parameters and the Bezier curve; (3) performing affine transformation according to the morphology of the hinge zone and the middle section to generate the sections at both ends of the fold; (4) generating transition sections of the 3D symbol model, based on morphing interpolation; and (5) connecting the point sets of each transition section and stitching them to obtain a 3D fold-symbol model. Case studies for different typical fold structures show that this method can eliminate excessive dependence on geological survey data in the modeling process and realize efficient, intuitive, and abstract 3D symbol modeling of fold structures based on only a few parameters. This method also applies to the 3D geological symbol modeling of faults, joints, intrusions, and other geological structures and 3D geological modeling of typical geological structures with a relatively simple spatial morphology.
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- 2022
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5. 3D Modeling Method for Dome Structure Using Digital Geological Map and DEM
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Xian-Yu Liu, An-Bo Li, Hao Chen, Yan-Qing Men, and Yong-Liang Huang
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three-dimensional geological modeling ,attitude calculation ,dome structure ,digital geological map ,interface generation ,Geography (General) ,G1-922 - Abstract
Geological maps have wide coverage with low acquisition difficulty. When other geological survey data are scarce, they are a valuable source of geological structure information for geological modeling. However, for structures with large deformation, geological map information has difficulty meeting the requirement of its 3D geological modeling. Therefore, this paper takes the dome structure as an example to explore a 3D modeling method based on geological maps, DEM and related geological knowledge. The method includes: (1) adaptively calculating the attitude of points on the stratigraphic boundaries; (2) inferring and generating the bottom boundary of the model from the attitude data of the boundary points; (3) generating the model interface constrained by Bézier curves based on the bottom boundary; (4) generating the top and bottom surfaces of the stratum; and (5) stitching each surface of the geological body to generate the final dome model. Case studies of the dome in Wulongshan in China and the Richat structure in Mauritania show that this method can build a solid model of the dome based only on geological maps and DEM data, whose morphological features are basically consistent with those embodied in the section view or the model generated by traditional methods.
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- 2022
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6. Non-canonical Opioid Signaling Inhibits Itch Transmission in the Spinal Cord of Mice
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Admire Munanairi, Xian-Yu Liu, Devin M. Barry, Qianyi Yang, Jun-Bin Yin, Hua Jin, Hui Li, Qing-Tao Meng, Jia-Hang Peng, Zhen-Yu Wu, Jun Yin, Xuan-Yi Zhou, Li Wan, Ping Mo, Seungil Kim, Fu-Quan Huo, Joseph Jeffry, Yun-Qing Li, Rita Bardoni, Michael R. Bruchas, and Zhou-Feng Chen
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Biology (General) ,QH301-705.5 - Abstract
Summary: Chronic itch or pruritus is a debilitating disorder that is refractory to conventional anti-histamine treatment. Kappa opioid receptor (KOR) agonists have been used to treat chronic itch, but the underlying mechanism remains elusive. Here, we find that KOR and gastrin-releasing peptide receptor (GRPR) overlap in the spinal cord, and KOR activation attenuated GRPR-mediated histamine-independent acute and chronic itch in mice. Notably, canonical KOR-mediated Gαi signaling is not required for desensitizing GRPR function. In vivo and in vitro studies suggest that KOR activation results in the translocation of Ca2+-independent protein kinase C (PKC)δ from the cytosol to the plasma membrane, which in turn phosphorylates and inhibits GRPR activity. A blockade of phospholipase C (PLC) in HEK293 cells prevented KOR-agonist-induced PKCδ translocation and GRPR phosphorylation, suggesting a role of PLC signaling in KOR-mediated GRPR desensitization. These data suggest that a KOR-PLC-PKCδ-GRPR signaling pathway in the spinal cord may underlie KOR-agonists-induced anti-pruritus therapies. : Munanairi et al. show that the kappa opioid receptor (KOR) agonists inhibit nonhistaminergic itch transmission by attenuating the function of the gastrin-releasing peptide receptor (GRPR), an itch receptor in the spinal cord. KOR activation causes the translocation of PKCδ from plasma to membrane, which phosphorylates GRPR to dampen itch transmission. Keywords: KOR, GRPR, itch, PKC, phosphorylation, GPCR cross-signaling, spinal cord, mouse
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- 2018
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7. Triptolide protects dopaminergic neurons from inflammation-mediated damage induced by lipopolysaccharide intranigral injection
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Hui-Fang Zhou, Xian-Yu Liu, Dong-Bin Niu, Feng-Qiao Li, Qi-Hua He, and Xiao-Min Wang
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Triptolide ,Tripterygium wilfordii Hook F ,Inflammation ,Microglia ,Parkinson's disease ,Neurodegeneration ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Converging lines of evidence suggest that neuroinflammatory processes may account for the progressive death of dopaminergic neurons in Parkinson's disease (PD). Therefore, anti-inflammatory strategies have attracted much interest for their potential to prevent further deterioration of PD. Our previous study showed that triptolide, a traditional Chinese herbal compound with anti-inflammatory and immunosuppressive properties, protected dopaminergic neurons from lipopolysaccharide (LPS)-induced damage in primary embryonic midbrain cell cultures. To examine further if triptolide can protect dopaminergic neurons from inflammation-mediated damage in vivo, microglial activation and injury of dopaminergic neurons were induced by LPS intranigral injection, and the effects of triptolide treatment on microglial activation and survival ratio and function of dopaminergic neurons were investigated. Our results demonstrated that microglial activation induced by a single intranigral dose of 10 μg of LPS reduced the survival ratio of tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the substantia nigra pars compacta (SNpc) to 29% and the content of dopamine (DA) in striatum to 37% of the non-injected side. Intriguingly, treatment with triptolide of 5 μg/kg for 24 days once per day dramatically improved the survival rate of TH-ir neurons in the SNpc to 79% of the non-injected side. Meanwhile, treatment with triptolide of 1 or 5 μg/kg for 24 days once per day significantly improved DA level in striatum to 70% and 68% of the non-injected side, respectively. Complement receptor 3 (CR3) immunohistochemical staining revealed that triptolide treatment potently inhibited LPS-elicited deleterious activation of microglia in SNpc. The excessive production of cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, was significantly abolished by triptolide administration. These results, together with our previous data in vitro, highly suggest the effectiveness of triptolide in protecting dopaminergic neurons against inflammatory challenge.
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- 2005
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8. Parametric Modeling Method for 3D Symbols of Fold Structures.
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Anbo Li, Hao Chen, Xiao-Feng Du, Guo-Kai Sun, and Xian-Yu Liu
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- 2022
- Full Text
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9. Characteristics of cyanobacteria pyrolysis and gasification during chemical looping process with red mud oxygen carrier
- Author
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Hai-feng ZHANG, Lu CHEN, Xian-yu LIU, Hui-jun GE, Tao SONG, and Lai-hong SHEN
- Published
- 2021
10. Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors
- Author
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Ailin Tao, Steven Wilhelm, Zhou-Feng Chen, Xiansi Zeng, Xue Ting Liu, Juan Liu, Jun Yin, Fang Gao, Ben-Long Liu, Qianyi Yang, Xian-Yu Liu, and Devin M. Barry
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0301 basic medicine ,General Physics and Astronomy ,Gene Knockout Techniques ,Mice ,chemistry.chemical_compound ,0302 clinical medicine ,Gastrin-releasing peptide ,Conditional gene knockout ,Medicine ,Neurotransmitter ,skin and connective tissue diseases ,lcsh:Science ,Skin ,Mice, Knockout ,Neurotransmitter Agents ,Multidisciplinary ,Chemogenetics ,medicine.anatomical_structure ,Gastrin-Releasing Peptide ,Spinal Cord ,Sensory processing ,hormones, hormone substitutes, and hormone antagonists ,Histamine ,Sensory Receptor Cells ,Science ,Pain ,Neuropeptide ,Sensory system ,Article ,General Biochemistry, Genetics and Molecular Biology ,03 medical and health sciences ,parasitic diseases ,otorhinolaryngologic diseases ,Animals ,business.industry ,Pruritus ,General Chemistry ,Scratching ,Spinal cord ,eye diseases ,Mice, Inbred C57BL ,Disease Models, Animal ,030104 developmental biology ,chemistry ,nervous system ,lcsh:Q ,Transcriptome ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Gastrin-releasing peptide (GRP) functions as a neurotransmitter for non-histaminergic itch, but its site of action (sensory neurons vs spinal cord) remains controversial. To determine the role of GRP in sensory neurons, we generated a floxed Grp mouse line. We found that conditional knockout of Grp in sensory neurons results in attenuated non-histaminergic itch, without impairing histamine-induced itch. Using a Grp-Cre knock-in mouse line, we show that the upper epidermis of the skin is exclusively innervated by GRP fibers, whose activation via optogeneics and chemogenetics in the skin evokes itch- but not pain-related scratching or wiping behaviors. In contrast, intersectional genetic ablation of spinal Grp neurons does not affect itch nor pain transmission, demonstrating that spinal Grp neurons are dispensable for itch transmission. These data indicate that GRP is a neuropeptide in sensory neurons for non-histaminergic itch, and GRP sensory neurons are dedicated to itch transmission., The role of gastrin related peptide (GRP+) neurons in itch is debated. Here, the authors generate a conditional knock-in mouse to label and manipulate GRP expressing DRG neurons and investigate their role in itch and nociception.
- Published
- 2020
11. Author response: BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk
- Author
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Juan Liu, Xue-Ting Liu, Xian-Yu Liu, Qing-Tao Meng, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
- Published
- 2021
12. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk
- Author
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Juan Liu, Xue-Ting Liu, Xian-Yu Liu, Qing-Tao Meng, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
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Male ,Mouse ,QH301-705.5 ,Neurokinin B ,Science ,NPRC ,NPRA ,General Biochemistry, Genetics and Molecular Biology ,Mice ,Ganglia, Spinal ,Natriuretic Peptide, Brain ,Animals ,Humans ,itch ,Biology (General) ,General Immunology and Microbiology ,General Neuroscience ,Pruritus ,spinal cord ,General Medicine ,Mice, Inbred C57BL ,HEK293 Cells ,Medicine ,GRP ,Receptors, Atrial Natriuretic Factor ,hormones, hormone substitutes, and hormone antagonists ,Histamine ,Signal Transduction ,Research Article ,Neuroscience ,BNP - Abstract
Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCβ-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice., eLife digest An itch is a common sensation that makes us want to scratch. Most short-term itches are caused by histamine, a chemical that is released by immune cells following an infection or in response to an allergic reaction. Chronic itching, on the other hand, is not usually triggered by histamine, and is typically the result of neurological or skin disorders, such as atopic dermatitis. The sensation of itching is generated by signals that travel from the skin to nerve cells in the spinal cord. Studies in mice have shown that the neuropeptides responsible for delivering these signals differ depending on whether or not the itch involves histamine: GRPs (short for gastrin-releasing proteins) convey histamine-independent itches, while NMBs (short for neuromedin B) convey histamine-dependent itches. It has been proposed that another neuropeptide called BNP (short for B-type natriuretic peptide) is able to transmit both types of itch signals to the spinal cord. But it remains unclear how this signaling molecule is able to do this. To investigate, Meng, Liu, Liu, Liu et al. carried out a combination of behavioral, molecular and pharmacological experiments in mice and nerve cells cultured in a laboratory. The experiments showed that BNP alone cannot transmit the sensation of itching, but it can boost itching signals that are triggered by histamine. It is widely believed that BNP activates a receptor protein called NPRA. However, Meng et al. found that the BNP actually binds to another protein which alters the function of the receptor activated by NMBs. These findings suggest that BNP modulates rather than initiates histamine-dependent itching by enhancing the interaction between NMBs and their receptor. Understanding how itch signals travel from the skin to neurons in the spinal cord is crucial for designing new treatments for chronic itching. The work by Meng et al. suggests that treatments targeting NPRA, which was thought to be a key itch receptor, may not be effective against chronic itching, and that other drug targets need to be explored.
- Published
- 2021
13. Vanadium Pentoxide Nanofibers/Carbon Nanotubes Hybrid Film for High-Performance Aqueous Zinc-Ion Batteries
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Qiongqiong Lu, Liwen Ma, Yehong Du, Xinyu Wang, Xian-Yu Liu, and Aikai Yang
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Battery (electricity) ,Materials science ,carbon nanotubes ,General Chemical Engineering ,aqueous zinc-ion battery ,Vanadium ,chemistry.chemical_element ,Carbon nanotube ,vanadium pentoxide ,hybrid film ,Energy storage ,Article ,law.invention ,Chemistry ,Chemical engineering ,chemistry ,law ,Nanofiber ,Electrode ,ddc:540 ,Ionic conductivity ,Pentoxide ,General Materials Science ,QD1-999 - Abstract
Aqueous zinc-ion batteries (ZIBs) with the characteristics of low production costs and good safety have been regarded as ideal candidates for large-scale energy storage applications. However, the nonconductive and non-redox active polymer used as the binder in the traditional preparation of electrodes hinders the exposure of active sites and limits the diffusion of ions, compromising the energy density of the electrode in ZIBs. Herein, we fabricated vanadium pentoxide nanofibers/carbon nanotubes (V2O5/CNTs) hybrid films as binder-free cathodes for ZIBs. High ionic conductivity and electronic conductivity were enabled in the V2O5/CNTs film due to the porous structure of the film and the introduction of carbon nanotubes with high electronic conductivity. As a result, the batteries based on the V2O5/CNTs film exhibited a higher capacity of 390 mAh g−1 at 1 A g−1, as compared to batteries based on V2O5 (263 mAh g−1). Even at 5 A g−1, the battery based on the V2O5/CNTs film maintained a capacity of 250 mAh g−1 after 2000 cycles with a capacity retention of 94%. In addition, the V2O5/CNTs film electrode also showed a high energy/power density (e.g., 67 kW kg−1/267 Wh kg−1). The capacitance response and rapid diffusion coefficient of Zn2+ (~10−8 cm−2 s−1) can explain the excellent rate capability of V2O5/CNTs. The vanadium pentoxide nanofibers/carbon nanotubes hybrid film as binder-free cathodes showed a high capability and a stable cyclability, demonstrating that it is highly promising for large-scale energy storage applications.
- Published
- 2021
14. BNP facilitates NMB-mediated histaminergic itch via NPRC-NMBR crosstalk
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Jun Yin, Ailin Tao, Admire Munanairi, Kai-Feng Shen, Devin M. Barry, Yu Sun, Hua Jin, Xian-Yu Liu, Qianyi Yang, Qing-Tao Meng, Jin-Hua Jin, Zhou-Feng Chen, Raymond J. Kim, Xue-Ting Liu, and Li Wan
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medicine.drug_class ,HEK 293 cells ,Histaminergic ,Neuropeptide ,Neuromedin B receptor ,Pharmacology ,chemistry.chemical_compound ,chemistry ,Gastrin-releasing peptide ,Natriuretic peptide ,medicine ,skin and connective tissue diseases ,Receptor ,hormones, hormone substitutes, and hormone antagonists ,Histamine - Abstract
B-type natriuretic peptide (BNP) binds to its two cognate receptors NPRA and NPRC, encoded by Npr1 and Npr3, respectively, with equal potency and both are expressed in the spinal cord. Moreover, natriuretic peptides (NP) signal through the inhibitory cGMP pathway, raising the question of how BNP may transmit itch information. We report that Npr3 is highly restricted to laminae I-II of the dorsal horn, and partially overlaps with neuromedin B receptor (NMBR) that encodes histaminergic itch. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not gastrin releasing peptide (GRP) that encodes nonhistaminergic itch. Consistently, BNP evoked Ca2+ response in NMBR/NPRC HEK 293 cells and BNP-saporin that ablated both Npr1 and Npr3 neurons impaired histamine-, but not CQ-evoked, itch. These results reveal a previously unknown mechanism by which BNP changes its inhibitory mode of action to the facilitation of itch through a novel NPRC-NMBR cross-talk. Our studies suggest that neuropeptides encode histaminergic and nonhistaminergic itch not only through distinct modes but also in synergy.
- Published
- 2021
15. Cellular basis of itch sensation
- Author
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Yan-Gang, Sun, Zhong-Qiu, Zhao, Xiu-Li, Meng, Jun, Yin, Xian-Yu, Liu, and Zhou-Feng, Chen
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Gastrin -- Properties ,Cell receptors -- Properties ,Spinal cord -- Genetic aspects ,Pruritus -- Genetic aspects ,Science and technology - Abstract
Itch and pain are two distinct sensations. Although our previous study suggested that gastrin-releasing peptide receptor (GRPR) is an itch-specific gene in the spinal cord, a long-standing question of whether there ate separate neuronal pathways for itch and pain remains unsettled. We selectively ablated lamina I neurons expressing GRPR in the spinal cord of mice. These mice showed profound scratching deficits in response to all of the itching (pruritogenic) stimuli tested, irrespective of their histamine dependence. In contrast, pain behaviors were unaffected. Our data also suggest that [GRPR.sup.+] neurons are different from the spinothalamic tract neurons that have been the focus of the debate. Together, the present study suggests that [GRPR.sup.+] neurons constitute a long-sought labeled line for itch sensation in the spinal cord.
- Published
- 2009
16. NPY2R signaling gates spontaneous and mechanical, but not thermal, pain transmission
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Xian-Yu Liu, Sihan Chen, Weifeng Yu, Yingfu Jiao, and Zhou-Feng Chen
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Male ,Pain ,NPY ,Arginine ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Mice ,0302 clinical medicine ,030202 anesthesiology ,Y1R ,medicine ,Animals ,Injections, Spinal ,business.industry ,Chronic pain ,spinal cord ,Benzazepines ,medicine.disease ,Spinal cord ,Neuropeptide Y receptor ,3. Good health ,Receptors, Neuropeptide Y ,Mice, Inbred C57BL ,Anesthesiology and Pain Medicine ,medicine.anatomical_structure ,Y2R ,Molecular Medicine ,Thermal pain ,business ,Neuroscience ,030217 neurology & neurosurgery ,Research Article - Abstract
Neuropeptide Y signaling plays an important role in inhibiting chronic pain in the spinal cord of mice. However, little is known about the respective roles of two major neuropeptide Y receptors, Y1R and Y2R, in evoked and spontaneous pain behavior under normal physiological condition. Using intrathecal administration approach, we found that pharmacological inhibition of Y2R, unexpectedly, gave rise to spontaneous pain behavior. In addition, Y2R antagonism also resulted in long-lasting mechanical but not thermal hypersensitivity. By contrast, neither overt spontaneous pain behavior nor mechanical and thermal hypersensitivity were detected after pharmacological inhibition of Y1R. Remarkably, the activation of Y1R produced powerful analgesic effect: blocking both evoked and spontaneous pain behavior resulted from Y2R antagonism. These findings highlight the pivotal role of endogenous Y2R in gating mechanical and spontaneous pain transmission. Importantly, our results suggest that Y1R could be a therapeutic target that may be exploited for alleviating spontaneous pain without affecting acute pain transmission.
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- 2019
17. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk.
- Author
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Qing-Tao Meng, Xian-Yu Liu, Xue-Ting Liu, Juan Liu, Munanairi, Admire, Barry, Devin M., Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
- Subjects
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ITCHING , *NATRIURETIC peptides , *NEURAL pathways , *PEPTIDES , *SPINAL cord , *NEUROPEPTIDES - Abstract
Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCß-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice. [ABSTRACT FROM AUTHOR]
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- 2022
- Full Text
- View/download PDF
18. PAR2 Mediates Itch via TRPV3 Signaling in Keratinocytes
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Jiahui Zhao, Xian-Yu Liu, Admire Munanairi, Meiqin Hu, Brian S. Kim, Lingling Liu, Zhou-Feng Chen, Dingfang Bu, Yong Yang, Zhiqiang Xie, Jie Zhang, and Linghan Hu
- Subjects
0301 basic medicine ,Keratinocytes ,Male ,TRPV3 ,Thymic stromal lymphopoietin ,Biopsy ,TRPV Cation Channels ,Dermatology ,Biochemistry ,Article ,Dermatitis, Atopic ,03 medical and health sciences ,Transient receptor potential channel ,Mice ,0302 clinical medicine ,Downregulation and upregulation ,medicine ,Animals ,Humans ,Receptor, PAR-2 ,skin and connective tissue diseases ,Receptor ,Molecular Biology ,Protease-activated receptor 2 ,Antipruritic ,Skin ,Mice, Knockout ,business.industry ,Pruritus ,Cell Biology ,Atopic dermatitis ,Antipruritics ,medicine.disease ,Up-Regulation ,Disease Models, Animal ,030104 developmental biology ,030220 oncology & carcinogenesis ,Gain of Function Mutation ,Immunology ,business ,medicine.drug ,Signal Transduction - Abstract
Animal studies have suggested that transient receptor potential (TRP) ion channels and G protein-coupled receptors (GPCRs) play important roles in itch transmission. TRPV3 gain-of-function mutations have been identified in patients with Olmsted syndrome which is associated with severe pruritus. However, the mechanisms causing itch remain poorly understood. Here, we show that keratinocytes lacking TRPV3 impair the function of protease activated receptor 2 (PAR2), resulting in reduced neuronal activation and scratching behavior in response to PAR2 agonists. Moreover, we show that TRPV3 and PAR2 were upregulated in skin biopsies from patients and mice with atopic dermatitis (AD), whereas their inhibition attenuated scratching and inflammatory responses in mouse AD models. Taken together, these results reveal a previously unrecognized link between TRPV3 and PAR2 in keratinocytes to convey itch information and suggest that a blockade of PAR2 or TRPV3 individually or both may serve as a potential approach for antipruritic therapy in AD.
- Published
- 2019
19. A spinal neural circuitry for converting touch to itch sensation
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Xian-Yu Liu, Yingfu Jiao, Devin M. Barry, Ben-Long Liu, Yufen Zhang, Kun Liu, Xiaofei Gao, Zhou-Feng Chen, Weifeng Yu, Sihan Chen, Yuxi Zhou, and Rita Bardoni
- Subjects
0301 basic medicine ,Peptide receptor ,Light ,Nerve net ,Neural substrate ,Molecular biology ,General Physics and Astronomy ,Membrane Potentials ,0302 clinical medicine ,immune system diseases ,lcsh:Science ,skin and connective tissue diseases ,Injections, Spinal ,Skin ,Neurons ,Multidisciplinary ,Behavior, Animal ,Mechanoreceptor ,medicine.anatomical_structure ,Spinal Cord ,Sensory processing ,Proto-Oncogene Proteins c-fos ,Science ,General Biochemistry, Genetics and Molecular Biology ,Article ,Animals ,Mice, Inbred C57BL ,Nerve Net ,Protein Precursors ,Pruritus ,Receptors, Bombesin ,Synapses ,Tachykinins ,Touch ,03 medical and health sciences ,Sensation ,parasitic diseases ,medicine ,Biological neural network ,otorhinolaryngologic diseases ,Neural correlates of consciousness ,business.industry ,General Chemistry ,Spinal cord ,eye diseases ,030104 developmental biology ,lcsh:Q ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Touch and itch sensations are crucial for evoking defensive and emotional responses, and light tactile touch may induce unpleasant itch sensations (mechanical itch or alloknesis). The neural substrate for touch-to-itch conversion in the spinal cord remains elusive. We report that spinal interneurons expressing Tachykinin 2-Cre (Tac2Cre) receive direct Aβ low threshold mechanoreceptor (LTMR) input and form monosynaptic connections with GRPR neurons. Ablation or inhibition markedly reduces mechanical but not acute chemical itch nor noxious touch information. Chemogenetic inhibition of Tac2Cre neurons also displays pronounced deficit in chronic dry skin itch, a type of chemical itch in mice. Consistently, ablation of gastrin-releasing peptide receptor (GRPR) neurons, which are essential for transmitting chemical itch, also abolishes mechanical itch. Together, these results suggest that innocuous touch and chemical itch information converge on GRPR neurons and thus map an exquisite spinal circuitry hard-wired for converting innocuous touch to irritating itch., Light touch can sometimes induce unpleasant itch sensation but the neural correlates of this conversion are not well studied. Here, the authors provide evidence that Tac2 expressing spinal interneurons are connected to gastrin-releasing peptide receptor (GRPR) neurons and form an integral part of the neural circuit underlying touch evoked itch.
- Published
- 2019
20. GRP and NMB: distinct functions in itch transmission
- Author
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Xian-Yu Liu, Zhou-Feng Chen, and Devin M. Barry
- Subjects
Transmission (mechanics) ,law ,Biology ,Neuroscience ,law.invention - Published
- 2021
21. [The Gemological Characteristics of One Kind Turquoise Imitation]
- Author
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Quan-li, Chen, Su-jie, Al, Qian-xiang, Wang, Xian-yu, Liu, Xin-rong, Ding, and Zuo-wei, Yin
- Abstract
It has been a long time that the imitations of turquoise appear in gem market. Pressed dyed carbonate in the early stage and dyed variscite, chalcedony as well as magnesite appeared in succession. These kinds of materials do not have the color and characteristics of natural turquoise. Their physical and optical properties are quite different from natural turquoise. One kind of turquoise imitation newly appears in market is selected to be studied in this paper. The conventional gemological method, infrared absorption spectroscopy and X-ray diffraction were employed to study its mineral compositions, gemological properties and structural characteristics. The results show that: the brecciated structure can be observed and the distribution of the iron wire is very simple on the surface of the sample. Deep blue granules are visible on the surface of blue samples and a few black spots can be observed on the surface of white ones, which are typical indication of pressing process. The blue imitations of turquoise has been stained and pressed. The index of this kind of turquoise imitation range from 1.54 to 1.58, which is lower than that of natural turquoise and it show bluish white fluorescence, which can be used as important evidence to distinguish it with natural turquoise. The data of X-ray diffraction shows the sample mainly consists of enstatite and quartz. The results of infrared absorption spectroscopy show that the absorption spectra of this kind of turquoise imitation is in accordance with the typical absorption peaks of enstatite: the absorption peaks which locates near 1 088 and 799 cm-1 are associated with Si—O, Si—O—Si stretching vibration in quartz; the absorption peaks near 2 947 and 2 882 cm-1 is related with stretching vibration of CH2 of exotic organic resin; the absorption peaks near 1 736 and 1 510 cm-1 are resulted from the bending and stretching vibration of CO and CH2.
- Published
- 2018
22. Exploration of Sensory and Spinal Neurons Expressing GRP in Itch and Pain
- Author
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Xian-Yu Liu, Zhou-Feng Chen, Qianyi Yang, Devin M. Barry, Ben-Long Liu, Xiansi Zeng, and Xue-Ting Liu
- Subjects
0303 health sciences ,Epidermis (botany) ,business.industry ,Channelrhodopsin ,Sensory system ,Scratching ,Spinal cord ,eye diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine.anatomical_structure ,Dorsal root ganglion ,chemistry ,parasitic diseases ,otorhinolaryngologic diseases ,Medicine ,skin and connective tissue diseases ,business ,Neurotransmitter ,Neuroscience ,hormones, hormone substitutes, and hormone antagonists ,030217 neurology & neurosurgery ,030304 developmental biology ,Pain transmission - Abstract
Gastrin-releasing peptide (GRP) is a putative itch-specific neurotransmitter, but definite evidence in the dorsal root ganglion (DRG) and spinal cord is lacking. We generated and validated a Grp-Cre knock-in (GrpCre-KI) mouse line whereby Grp neurons are genetically labeled. Cre-dependent marking analysis revealed exclusive innervation of the upper epidermis of the skin by GRP fibers. Importantly, optical stimulation of Grp fibers expressing channel rhodopsin (ChR2) in the skin evoked itch but not pain-related scratching behaviors, while conditional deletion of Grp in sensory neurons attenuated non-histaminergic itch. In contrast, intersectional genetic ablation of spinal Grp neurons did not affect itch nor pain transmission. Our study demonstrates a role of GRP in sensory neurons in itch and suggests that GRP sensory neurons are dedicated to itch transmission. GrpCre-KI mice provide a long-sought avenue for investigating peripheral coding mechanism of itch and further interrogation of itch-nerve fibers in the skin under chronic pruritus.HighlightsValidated expression of a Grp-Cre knock-in line in sensory neurons that innervate the skinOpto-activation of Grp sensory neurons evokes itch behaviorConditional deletion of Grp in sensory neurons reduces non-histaminergic itch behaviorIntersectional ablation of Grp spinal neurons does not affect itch or pain behaviors
- Published
- 2018
23. Cross-Talk between Distinct Receptors Shapes Itch Behavior in the Spinal Cord
- Author
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Ailin Tao, Qianyi Yang, Qing-Tao Meng, Zhou-Feng Chen, Jin-Hua Jin, Devin M. Barry, Li Wan, Admire Munanairi, Xue-Ting Liu, Ray Kim, Jun Yin, Yu Sun, Hua Jin, and Xian-Yu Liu
- Subjects
chemistry.chemical_classification ,medicine.drug_class ,Peptide ,Neuromedin B receptor ,Scratching ,NPR1 ,Spinal cord ,Cell biology ,chemistry.chemical_compound ,medicine.anatomical_structure ,chemistry ,Natriuretic peptide ,medicine ,skin and connective tissue diseases ,Receptor ,hormones, hormone substitutes, and hormone antagonists ,Histamine - Abstract
Natriuretic peptide (NP) family comprises multiple peptides/receptors whose respective role in itch transmission remains unclear. We report that about 23% of Npr1 that encodes NP receptor A (NPRA) in the superficial spinal cord co-express gastrin-releasing peptide (Grp), while Npr3 that encodes NP receptor C (NPRC), partially overlaps with the neuromedin B receptor (NMBR) required for histamine-evoked itch. While Npr1 is required for chloroquine- (CQ) and histamine-evoked itch, the role of Npr3 is limited to the latter. Notably, B-type natriuretic peptide (BNP) significantly facilitated NMB-, but not GRP-, evoked scratching behavior, and Ca2 response in NMBR/NPRC cells. Consistently, BNP-saporin ablated spinal Npr1 and Npr3 neurons and impaired histamine-, but not CQ-evoked, itch. Thus, the findings identify the role of BNP-NPRC signaling in modulation of histamine-evoked itch via NPRC-NMBR cross-talk independent of GRP-GRPR signaling. Our studies reveal distinct modes of action for bombesin-related peptides and NP in itch transmission.
- Published
- 2018
24. Distinct roles of NMB and GRP in itch transmission
- Author
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Xian-Yu Liu, Jin Hua Jin, Devin M. Barry, Hua Jin, Ailin Tao, Zhou-Feng Chen, Jia Hang Peng, Ray Kim, Xue Ting Liu, Joseph Jeffry, Qing Tao Meng, Jun Yin, Ping Mo, Yu Sun, Rita Bardoni, Kai Feng Shen, and Li Wan
- Subjects
0301 basic medicine ,Male ,Nociception ,Neurokinin B ,lcsh:Medicine ,Biology ,Article ,03 medical and health sciences ,chemistry.chemical_compound ,Glutamatergic ,Mice ,0302 clinical medicine ,parasitic diseases ,Biological neural network ,Noxious stimulus ,otorhinolaryngologic diseases ,Animals ,Humans ,lcsh:Science ,Neurotransmitter ,Receptor ,skin and connective tissue diseases ,Skin ,Mice, Knockout ,Multidisciplinary ,Behavior, Animal ,Pruritus ,lcsh:R ,Bombesin ,Nociceptors ,Antipruritics ,Neuromedin B ,eye diseases ,Mice, Inbred C57BL ,Receptors, Bombesin ,Electrophysiology ,Disease Models, Animal ,030104 developmental biology ,chemistry ,Gastrin-Releasing Peptide ,Spinal Cord ,lcsh:Q ,Capsaicin ,Neuroscience ,030217 neurology & neurosurgery ,hormones, hormone substitutes, and hormone antagonists ,Histamine ,Signal Transduction - Abstract
A key question in our understanding of itch coding mechanisms is whether itch is relayed by dedicated molecular and neuronal pathways. Previous studies suggested that gastrin-releasing peptide (GRP) is an itch-specific neurotransmitter. Neuromedin B (NMB) is a mammalian member of the bombesin family of peptides closely related to GRP, but its role in itch is unclear. Here, we show that itch deficits in mice lacking NMB or GRP are non-redundant and Nmb/Grp double KO (DKO) mice displayed additive deficits. Furthermore, both Nmb/Grp and Nmbr/Grpr DKO mice responded normally to a wide array of noxious stimuli. Ablation of NMBR neurons partially attenuated peripherally induced itch without compromising nociceptive processing. Importantly, electrophysiological studies suggested that GRPR neurons receive glutamatergic input from NMBR neurons. Thus, we propose that NMB and GRP may transmit discrete itch information and NMBR neurons are an integral part of neural circuits for itch in the spinal cord.
- Published
- 2017
25. B-Type Natriuretic Peptide is Neither Itch-Specific Nor Functions Upstream of the GRP-GRPR Signaling Pathway
- Author
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Devin M. Barry, Li Wan, Fu-Quan Huo, Hui Li, Zhou-Feng Chen, Zhong Qiu Zhao, and Xian-Yu Liu
- Subjects
Male ,medicine.medical_specialty ,medicine.drug_class ,GRPR ,Short Report ,Pain ,In situ hybridization ,NPRA ,Itch ,Mice ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Dorsal root ganglion ,Ganglia, Spinal ,Gastrin-releasing peptide ,Internal medicine ,Natriuretic Peptide, Brain ,Natriuretic peptide ,Animals ,Medicine ,RNA, Messenger ,Neurotransmitter ,Receptor ,Inflammation ,Spinal cord ,business.industry ,Pruritus ,Mice, Inbred C57BL ,Receptors, Bombesin ,Anesthesiology and Pain Medicine ,Endocrinology ,medicine.anatomical_structure ,Gastrin-Releasing Peptide ,Gene Expression Regulation ,chemistry ,DRG ,GRP ,Molecular Medicine ,Signal transduction ,business ,Receptors, Atrial Natriuretic Factor ,hormones, hormone substitutes, and hormone antagonists ,Immunostaining ,Signal Transduction ,BNP - Abstract
A recent study by Mishra and Hoon identified B-type natriuretic peptide (BNP) as an important peptide for itch transmission and proposed that BNP activates spinal natriuretic peptide receptor-A (NPRA) expressing neurons, which release gastrin releasing peptide (GRP) to activate GRP receptor (GRPR) expressing neurons to relay itch information from the periphery to the brain (Science 340:968–971, 2013). A central premise for the validity of this novel pathway is the absence of GRP in the dorsal root ganglion (DRG) neurons. To this end, they showed that Grp mRNA in DRG neurons is either absent or barely detectable and claimed that BNP but not GRP is a major neurotransmitter for itch in pruriceptors. They showed that NPRA immunostaining is perfectly co-localized with Grp-eGFP in the spinal cord, and a few acute pain behaviors in Nppb -/- mice were tested. They claimed that BNP is an itch-selective peptide that acts as the first station of a dedicated neuronal pathway comprising a GRP-GRPR cascade for itch. However, our studies, along with the others, do not support their claims. We were unable to reproduce the immunostaining of BNP and NPRA as shown by Mishra and Hoon. By contrast, we were able to detect Grp mRNA in DRGs using in situ hybridization and real time RT-PCR. We show that the expression pattern of Grp mRNA is comparable to that of GRP protein in DRGs. Pharmacological and genetic blockade of GRP-GRPR signaling does not significantly affect intrathecal BNP-induced scratching behavior. We show that BNP inhibits inflammatory pain and morphine analgesia. Accumulating evidence demonstrates that GRP is a key neurotransmitter in pruriceptors for mediating histamine-independent itch. BNP-NPRA signaling is involved in both itch and pain and does not function upstream of the GRP-GRPR dedicated neuronal pathway. The site of BNP action in itch and pain and its relationship with GRP remain to be clarified.
- Published
- 2014
26. NPY2R signaling gates spontaneous and mechanical, but not thermal, pain transmission.
- Author
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Sihan Chen, Xian-Yu Liu, Yingfu Jiao, Zhou-Feng Chen, and Weifeng Yu
- Subjects
- *
NEUROPEPTIDE Y receptors , *NEUROPEPTIDE Y , *CHRONIC pain , *PAIN , *SPINAL cord - Abstract
Neuropeptide Y signaling plays an important role in inhibiting chronic pain in the spinal cord of mice. However, little is known about the respective roles of two major neuropeptide Y receptors, Y1R and Y2R, in evoked and spontaneous pain behavior under normal physiological condition. Using intrathecal administration approach, we found that pharmacological inhibition of Y2R, unexpectedly, gave rise to spontaneous pain behavior. In addition, Y2R antagonism also resulted in longlasting mechanical but not thermal hypersensitivity. By contrast, neither overt spontaneous pain behavior nor mechanical and thermal hypersensitivity were detected after pharmacological inhibition of Y1R. Remarkably, the activation of Y1R produced powerful analgesic effect: blocking both evoked and spontaneous pain behavior resulted from Y2R antagonism. These findings highlight the pivotal role of endogenous Y2R in gating mechanical and spontaneous pain transmission. Importantly, our results suggest that Y1R could be a therapeutic target that may be exploited for alleviating spontaneous pain without affecting acute pain transmission. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
27. Research on Vibration Bench of Vehicle Suspension by Finite Element
- Author
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Xian Yu Liu
- Subjects
Vibration ,Stress field ,Engineering ,Mathematical model ,business.industry ,General Medicine ,Structural engineering ,business ,Suspension (vehicle) ,Finite element method - Abstract
By establishing and analyzing mathematical model for vibration bench of vehicle suspension, this paper optimized and simulated vibration bench of vehicle suspension based on finite element. As a result, the paper got stress field and its distribution during transformation process and set a foundation for structural design of vibration bench of suspension.
- Published
- 2013
28. Twin and topotactic growth of β-eucryptite dendrites and their lattice coincidence analysed by the reticular theory
- Author
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Xian-Yu Liu, Shan-Rong Zhao, Hai-Jun Xu, Qin-Yan Wang, and Rong Liu
- Subjects
Crystallography ,Materials science ,Lattice (order) ,Crystal morphology ,Crystal twinning ,Reticular theory ,General Biochemistry, Genetics and Molecular Biology ,Coincidence ,Solid solution - Abstract
Snowflake-shaped dendrites of β-eucryptite–β-quartz solid solution were artificially crystallized in a matt glaze, and the crystallographic orientation of the dendrites was analysed by the electron backscatter diffraction (EBSD) technique. The six branches of a snowflake-shaped dendrite in the plane (0001) are along 〈110〉. From the orientation determination, a twin relationship and a topotactic relationship between dendrites were found. The twin axes are [011], [0{\overline 1}1] and [210], and the twin planes perpendicular to the twin axes are ({\overline 1}2{\overline 1}2) and (1{\overline 2}12). From the reticular theory of twinning, it was calculated that the twin indexn= 2 and the obliquity ω = 3.2877°. The studied dendrite is a twin by reticular pseudomerohedry with low twin index and obliquity. In the topotactic growth, no twin elements have been found, but the three main crystallographic directions 〈001〉, 〈210〉 and 〈110〉 of the two dendritic crystals overlap each other. The degree of lattice coincidence between the two crystals in this topotactic growth is also discussed.
- Published
- 2013
29. Development of Engine Vibration Test Virtual Instrument
- Author
-
Xian Yu Liu
- Subjects
Automotive engine ,Vibration ,Engineering ,Software ,Data acquisition ,business.industry ,Fast Fourier transform ,Data recording ,General Medicine ,business ,Virtual instrument ,Computer hardware ,Test (assessment) - Abstract
Using the software technologies of the LabVIEW 7 Express and hardware technologies of the PCI-MIO-16E-4 data acquisition card, which is the famous production of NI designing and developing the Virtual Instrument about the engine vibration's real-time testing and analysis, including the vibration graphic displaying, data recording and the FFT of the engine vibration; Applying it to a automobile engine's base vibration, supplying a convenient condition for the performance analysis and default diagnosis of the engine.
- Published
- 2013
30. Facilitation of TRPV4 by TRPV1 is required for itch transmission in some sensory neuron populations
- Author
-
Devin M. Barry, Shen Bin Liu, Narasimhan Gautam, Qing Tao Meng, Zhong Qiu Zhao, Ping Mo, Zhou-Feng Chen, Jie Zheng, W. K. Ajith Karunarathne, Admire Munanairi, Seung Il Kim, Li Wan, Shijin Yin, Wei Cheng, Kasun Ratnayake, and Xian-Yu Liu
- Subjects
Male ,0301 basic medicine ,Sensory Receptor Cells ,TRPV1 ,TRPV Cation Channels ,Sensory system ,Pharmacology ,Somatosensory system ,Biochemistry ,Article ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,Transient receptor potential channel ,0302 clinical medicine ,Dorsal root ganglion ,Ganglia, Spinal ,medicine ,Animals ,Humans ,Calcium Signaling ,Molecular Biology ,Mice, Knockout ,Chemistry ,Pruritus ,musculoskeletal, neural, and ocular physiology ,Cell Biology ,Sensory neuron ,Cell biology ,HEK293 Cells ,030104 developmental biology ,medicine.anatomical_structure ,nervous system ,lipids (amino acids, peptides, and proteins) ,psychological phenomena and processes ,030217 neurology & neurosurgery ,Histamine - Abstract
The transient receptor potential channels (TRPs) respond to chemical irritants and temperature. TRPV1 responds to the itch-inducing endogenous signal histamine, and TRPA1 responds to the itch-inducing chemical chloroquine. We showed that, in sensory neurons, TRPV4 is important for both chloroquine- and histamine-induced itch and that TRPV1 has a role in chloroquine-induced itch. Chloroquine-induced scratching was reduced in mice in which TRPV1 was knocked down or pharmacologically inhibited. Both TRPV4 and TRPV1 were present in some sensory neurons. Pharmacological blockade of either TRPV4 or TRPV1 significantly attenuated the Ca(2+) response of sensory neurons exposed to histamine or chloroquine. Knockout of Trpv1 impaired Ca(2+) responses and reduced scratching behavior evoked by a TRPV4 agonist, whereas knockout of Trpv4 did not alter TRPV1-mediated capsaicin responses. Electrophysiological analysis of human embryonic kidney (HEK) 293 cells coexpressing TRPV4 and TRPV1 revealed that the presence of both channels enhanced the activation kinetics of TRPV4 but not of TRPV1. Biochemical and biophysical studies suggested a close proximity between TRPV4 and TRPV1 in dorsal root ganglion neurons and in cultured cells. Thus, our studies identified TRPV4 as a channel that contributes to both histamine- and chloroquine-induced itch and indicated that the function of TRPV4 in itch signaling involves TRPV1-mediated facilitation. TRP facilitation through the formation of heteromeric complexes could be a prevalent mechanism by which the vast array of somatosensory information is encoded in sensory neurons.
- Published
- 2016
31. [Study on Vibrational Spectra Characteristics of Gem-Quality Natrolite]
- Author
-
Xian-yu, Liu, Xi-tian, Shen, Ren, Lu, and Shan-rong, Zhao
- Abstract
Recently, there is a batch of colorless faceted gem-quality natrolite appear in the international jewelry market. In order to provide some information that can help us to distinguish them from the imitations. The infrared spectrometer and Raman spectrometer were employed to study the characteristics of the vibrational spectrum of three natrolite samples in this article. The typical infrared spectra shows that: the absorption region 4000~1200 cm(-1) is induced by stretching vibration of the hydroxyl group, the strong absorption peaks range from 1200~600 cm(-1) are relative with the anti-symmetry and symmetry stretching vibration of tetrahedral T-O bonds (T=Si or Al). The Raman spectra scattering peaks are located in the range of 300~600 and 700~1200 cm(-1). The low intensity Raman scattering spectrum in the range of 300~360 cm(-1) corresponds to the vibration of the water molecules in the crystal. The medium intensity Raman scattering spectrum is assigned to the deformation of SiO4 tetrahedra. The Raman spectra scattering peak at 726 cm(-1) is assigned to the stretching vibration of Al-O; The Si-O stretching vibration displays the Raman spectra scattering peaks at 974, 1038 and 1084 cm(-1).
- Published
- 2015
32. Activity-Dependent Modulation of Limbic Dopamine D3 Receptors by CaMKII
- Author
-
Hui Fang Zhou, Guo Chi Zhang, Hong Xiang Lan, Christopher J. Papasian, Eugene E. Fibuch, Xian-Yu Liu, John Q. Wang, Ming Xu, and Limin Mao
- Subjects
Male ,Dopamine ,Neuroscience(all) ,Synaptic Membranes ,HUMDISEASE ,Biology ,Neurotransmission ,Binding, Competitive ,Synaptic Transmission ,Nucleus Accumbens ,MOLNEURO ,03 medical and health sciences ,Cocaine-Related Disorders ,Mice ,0302 clinical medicine ,Dopamine receptor D3 ,Ca2+/calmodulin-dependent protein kinase ,medicine ,Limbic System ,Animals ,Calcium Signaling ,Phosphorylation ,Rats, Wistar ,030304 developmental biology ,Calcium signaling ,Mice, Knockout ,0303 health sciences ,Psychomotor function ,Binding Sites ,General Neuroscience ,Autophosphorylation ,Receptors, Dopamine D3 ,Cell biology ,Protein Structure, Tertiary ,Rats ,Dopamine receptor ,SIGNALING ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,Neuroscience ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is central to synaptic transmission. Here we show that synaptic CaMKIIalpha binds to the N-terminal region of the third intracellular loop of the limbic dopamine D3 receptor (D3R). This binding is Ca(2+) sensitive and is sustained by autophosphorylation of CaMKII, providing an unrecognized route for the Ca(2+)-mediated regulation of D3Rs. The interaction of CaMKIIalpha with D3Rs transforms D3Rs into a biochemical substrate of the kinase and promotes the kinase to phosphorylate D3Rs at a selective serine site (S229). In accumbal neurons in vivo, CaMKIIalpha is recruited to D3Rs by rising Ca(2+) to increase the CaMKIIalpha-mediated phosphorylation of D3Rs, thereby transiently inhibiting D3R efficacy. Notably, the D3R inhibition is critical for integrating dopamine signaling to control behavioral sensitivity to the psychostimulant cocaine. Our data identify CaMKIIalpha as a recruitable regulator of dopamine receptor function. By binding and phosphorylating limbic D3Rs, CaMKIIalpha modulates dopamine signaling and psychomotor function in an activity-dependent manner.
- Published
- 2009
- Full Text
- View/download PDF
33. Phosphorylation of group I metabotropic glutamate receptors (mGluR1/5) in vitro and in vivo
- Author
-
Eugene E. Fibuch, Zhenguo Liu, Xian-Yu Liu, Guo Chi Zhang, Xiang-Ping Chu, Limin Mao, Lucy S. Wang, and John Q. Wang
- Subjects
Pharmacology ,Metabotropic glutamate receptor 5 ,Receptor, Metabotropic Glutamate 5 ,Metabotropic glutamate receptor 4 ,Metabotropic glutamate receptor 7 ,Metabotropic glutamate receptor 6 ,Class C GPCR ,In Vitro Techniques ,Biology ,Receptors, Metabotropic Glutamate ,Article ,Cell biology ,Cellular and Molecular Neuroscience ,Biochemistry ,Metabotropic glutamate receptor ,Animals ,Humans ,Metabotropic glutamate receptor 1 ,Protein phosphorylation ,Phosphorylation - Abstract
Group I metabotropic glutamate receptors (mGluR1 and mGluR5 subtypes) are densely expressed in mammalian brain. They are actively involved in the regulation of normal cellular activity and synaptic plasticity, and are frequently linked to the pathogenesis of various mental illnesses. Like ionotropic glutamate receptors, group I mGluRs are subject to the regulation by protein phosphorylation. Accumulative data demonstrate sufficient phosphorylation of the intracellular mGluR1/5 domains at specific serine/threonine sites by protein kinase C in heterologous cells or neurons, which serves as an important mechanism for regulating the receptor signaling and desensitization. Emerging evidence also shows the significant involvements of G protein-coupled receptor kinases, Ca2+/calmodulin-dependent protein kinase II, tyrosine kinases, and protein phosphatases in controlling the phosphorylation status of group I mGluRs. This review analyzes the recent data concerning group I mGluR phosphorylation and the phosphorylation-dependent regulation of group I mGluR function. Future research directions in this area with newly available high throughput and proteomic approaches are also discussed in the end.
- Published
- 2008
34. Therapeutic Strategies for Parkinson’s Disease: The Ancient Meets the Future—Traditional Chinese Herbal Medicine, Electroacupuncture, Gene Therapy and Stem Cells
- Author
-
Xuan Wang, Jian-jun Wang, Hui Fang Zhou, Xiaomin Wang, Feng Qiao Li, Xian-Yu Liu, and Xi Bin Liang
- Subjects
medicine.medical_specialty ,Parkinson's disease ,Neurology ,Genetic enhancement ,MEDLINE ,Alternative medicine ,Disease ,Biochemistry ,Cellular and Molecular Neuroscience ,medicine ,Acupuncture ,Animals ,Humans ,Medicine, Chinese Traditional ,Intensive care medicine ,Traditional medicine ,Glutamate Decarboxylase ,business.industry ,Parkinson Disease ,Genetic Therapy ,General Medicine ,Phenanthrenes ,medicine.disease ,Electroacupuncture ,Epoxy Compounds ,Diterpenes ,Stem cell ,business ,Stem Cell Transplantation - Abstract
In China, it has been estimated that there are more than 2.0 million people suffering from Parkinson's disease, which is currently becoming one of the most common chronic neurodegenerative disorders during recent years. For many years, scientists have struggled to find new therapeutic approaches for this disease. Since 1994, our research group led by Drs. Ji-Sheng Han and Xiao-Min Wang of Neuroscience Research Institute, Peking University has developed several prospective treatment strategies for the disease. These studies cover the traditional Chinese medicine-herbal formula or acupuncture, and modern technologies such as gene therapy or stem cell replacement therapy, and have achieved some original results. It hopes that these data may be beneficial for the research development and for the future clinical utility for treatment of Parkinson's disease.
- Published
- 2008
35. Group I Metabotropic Glutamate Receptor-mediated Gene Expression in Striatal Neurons
- Author
-
Limin Mao, Guo Chi Zhang, John Q. Wang, Eugene E. Fibuch, and Xian-Yu Liu
- Subjects
MAPK/ERK pathway ,Dopamine ,Biology ,Receptors, Metabotropic Glutamate ,CREB ,Medium spiny neuron ,Biochemistry ,Immediate-Early Proteins ,Methoxyhydroxyphenylglycol ,Cellular and Molecular Neuroscience ,Homer Scaffolding Proteins ,Gene expression ,Animals ,Calcium Signaling ,Extracellular Signal-Regulated MAP Kinases ,Transcription factor ,Neurons ,Signal transducing adaptor protein ,General Medicine ,Molecular biology ,Corpus Striatum ,Cell biology ,Gene Expression Regulation ,biology.protein ,Metabotropic glutamate receptor 1 ,Mitogen-Activated Protein Kinases ,Carrier Proteins ,Immediate early gene ,Transcription Factors - Abstract
Group I mGluRs (mGluR1/5) are G-protein-coupled receptors and are abundantly expressed in most of medium spiny projection neurons in the striatum. Recent evidence demonstrates that group I mGluRs are among essential regulators for constitutive and inducible gene expression in host neurons. Upon activation, mGluR1/5 signals activate extracellular signal-regulated kinases (ERKs) which in turn phosphorylate transcription factors such as cAMP response element-binding protein (CREB) and Elk-1, and thereby facilitate immediate early gene and opioid peptide gene expression. The conventional mGluR1/5 signaling cascade (phosphoinositide hydrolysis and intracellular Ca(2+) release) participates in linking mGluR1/5 to ERK. Additionally, the prominent mGluR1/5 adaptor protein Homer contributes to assemble an efficient signaling apparatus connecting mGluR1/5 to gene expression. The mGluR1/5 linkage to transcription also functions in dopamine-stimulated gene expression. Together, the mGluR1/5-mediated gene expression constitutes a transcription-dependent mechanism underlying molecular adaptations and plasticity related to the pathogenesis of various mental illnesses.
- Published
- 2008
36. Cocaine increases Ras-guanine nucleotide-releasing factor 1 protein expression in the rat striatum in vivo
- Author
-
Jason Hoffmann, Nikhil K. Parelkar, Limin Mao, John Q. Wang, Guochi Zhang, Eugene E. Fibuch, and Xian-Yu Liu
- Subjects
Male ,MAPK/ERK pathway ,medicine.medical_specialty ,MAP Kinase Signaling System ,Striatum ,Nucleus accumbens ,Biology ,Cocaine-Related Disorders ,Ras-GRF1 ,Cocaine ,Dopamine Uptake Inhibitors ,Internal medicine ,Basal ganglia ,medicine ,Animals ,Rats, Wistar ,Protein kinase A ,Dose-Response Relationship, Drug ,ras-GRF1 ,Activator (genetics) ,General Neuroscience ,Corpus Striatum ,Rats ,Endocrinology ,Synaptic plasticity ,ras Guanine Nucleotide Exchange Factors - Abstract
Psychostimulants activate the Ras-mitogen-activated protein kinase (Ras-MAPK) cascade in the limbic reward circuit and thereby trigger a transcription-dependent mechanism underlying enduring synaptic plasticity related to addictive properties of drugs of abuse. The Ras-specific activator, Ras-guanine nucleotide-releasing factor (Ras-GRF), is predominantly expressed at synapses and is thought to actively regulate Ras-MAPK responses to changing synaptic signals. In this study, a possible influence of cocaine on Ras-GRF gene expression at the protein level in the rat striatum was investigated in vivo. A single systemic injection of cocaine induced an increase in Ras-GRF1 protein levels in both the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum. The increase in Ras-GRF1 proteins was dose-dependent and was a delayed and transient event. In contrast to Ras-GRF1, a closely related Ras-GRF2 showed no change in its protein abundance following cocaine administration. These data identify the Ras activator, Ras-GRF1, although not Ras-GRF2, as a susceptible target to cocaine stimulation in striatal neurons.
- Published
- 2007
37. C–H···Ni II Interaction‐Driven Homochiral M and P Helices of Neutral ( R , R )‐ and ( S , S )‐Bis(pyrrol‐2‐ylmethyleneamino)cyclohexane Ni II Complexes
- Author
-
Li-Zhu Wu, Li-Ping Zhang, Xian-Yu Liu, Xu-Feng Shan, and Chen-Ho Tung
- Subjects
Inorganic Chemistry ,chemistry.chemical_compound ,Nickel ,Crystallography ,Cyclohexane ,chemistry ,Stereochemistry ,chemistry.chemical_element ,Crystal structure ,Enantiomer - Abstract
Reaction of (R,R)- and (S,S)-bis(pyrrol-2-ylmethyleneamino)cyclohexane with NiII(OAc)2·4H2O afforded enantiomeric nickel(II) Schiff-base complexes (R,R)-1 and (S,S)-1, respectively. Rare C–H···NiII interactions were found to be responsible for the facile formation of homochiral M and P helices of the neutral, chiral, mononuclear complexes in crystal lattices. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
- Published
- 2007
38. A Signaling Mechanism from Gαq-Protein-Coupled Metabotropic Glutamate Receptors to Gene Expression: Role of the c-Jun N-Terminal Kinase Pathway
- Author
-
John Q. Wang, Xian-Yu Liu, Michael Catavsan, Hai Chen, Lu Yang, Jonathan Kozinn, Limin Mao, and Anish Arora
- Subjects
Receptor, Metabotropic Glutamate 5 ,Glutamic Acid ,Mitogen-activated protein kinase kinase ,Receptors, Metabotropic Glutamate ,Methoxyhydroxyphenylglycol ,mental disorders ,Animals ,Phosphorylation ,Cells, Cultured ,Dose-Response Relationship, Drug ,MAP kinase kinase kinase ,Chemistry ,General Neuroscience ,Metabotropic glutamate receptor 4 ,c-jun ,Metabotropic glutamate receptor 7 ,JNK Mitogen-Activated Protein Kinases ,Metabotropic glutamate receptor 6 ,Molecular biology ,Rats ,Gene Expression Regulation ,nervous system ,Metabotropic glutamate receptor ,GTP-Binding Protein alpha Subunits, Gq-G11 ,Metabotropic glutamate receptor 1 ,Cellular/Molecular ,Signal Transduction - Abstract
Gαq-protein-coupled group I metabotropic glutamate receptors (mGluRs) are densely expressed in brain neurons and are actively involved in various cellular activities. In this study, we investigated the role of group I mGluRs in regulating the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase in cultured neurons. We found that selective activation of mGluR5 induced a rapid and transient phosphorylation of JNK. In a series of studies to determine the mechanisms, we found that the conventional mGluR5-associated signaling pathways (inositol-1,4,5-triphosphate-mediated Ca2+release and activation of protein kinase C) were not involved in the mGluR5 regulation. Instead, ligand stimulation of mGluR5 caused a dynamic transactivation of the epidermal growth factor (EGF) receptor, which in turn triggered a downstream signaling pathway to upregulate JNK phosphorylation. Furthermore, the mGluR5-dependent JNK activation specifically activated c-Jun, but not activating transcription factor-2 or JunD, and increased activator protein-1 (AP-1)-mediated endogenous transcriptional activity. Together, we identified a novel mGluR5-to-nucleus communication through the EGF/JNK pathway, which functions to regulate AP-1-mediated transcription.
- Published
- 2006
39. Electro-acupuncture stimulation protects dopaminergic neurons from inflammation-mediated damage in medial forebrain bundle-transected rats
- Author
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Xiaomin Wang, Xian-Yu Liu, Xi-Bin Liang, Qi-Hua He, Xin-Hong Wang, Yan-Li Pan, Dong-Bin Niu, Hui-Fang Zhou, Bing Xue, and Feng-Qiao Li
- Subjects
medicine.medical_specialty ,Dopamine ,Acupuncture Therapy ,Macrophage-1 Antigen ,Cell Count ,Substantia nigra ,Stimulation ,Midbrain ,Random Allocation ,Developmental Neuroscience ,Internal medicine ,medicine ,Animals ,RNA, Messenger ,Rats, Wistar ,Medial forebrain bundle ,Neurons ,Analysis of Variance ,Cell Death ,Microglia ,biology ,Reverse Transcriptase Polymerase Chain Reaction ,Tumor Necrosis Factor-alpha ,Pars compacta ,Dopaminergic ,Medial Forebrain Bundle ,Membrane Proteins ,Axotomy ,Ectodysplasins ,Immunohistochemistry ,Electric Stimulation ,Rats ,Substantia Nigra ,medicine.anatomical_structure ,Endocrinology ,nervous system ,Neurology ,biology.protein ,Encephalitis ,Female ,Acupuncture Points ,Neuroscience ,Interleukin-1 ,Neurotrophin - Abstract
Through producing a variety of cytotoxic factors upon activation, microglia are believed to participate in the mediation of neurodegeneration. Intervention against microglial activation may therefore exert a neuroprotective effect. Our previous study has shown that the electro-acupuncture (EA) stimulation at 100 Hz can protect axotomized dopaminergic neurons from degeneration. To explore the underlying mechanism, the effects of 100 Hz EA stimulation on medial forebrain bundle (MFB) axotomy-induced microglial activation were investigated. Complement receptor 3 (CR3) immunohistochemical staining revealed that 24 sessions of 100 Hz EA stimulation (28 days after MFB transection) significantly inhibited the activation of microglia in the substantia nigra pars compacta (SNpc) induced by MFB transection. Moreover, 100 Hz EA stimulation obviously inhibited the upregulation of the levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta mRNA in the ventral midbrains in MFB-transected rats, as revealed by reverse transcriptase polymerase chain reaction (RT-PCR). ED1 immunohistochemical staining showed that a large number of macrophages appeared in the substantia nigra (SN) 14 days after MFB transection. The number of macrophages decreased by 47% in the rats that received 12 sessions of EA simulation after MFB transection. These data indicate that the neuroprotective role of 100 Hz EA stimulation on dopaminergic neurons in MFB-transected rats is likely to be mediated by suppressing axotomy-induced inflammatory responses. Taken together with our previous results, this study suggests that the neuroprotective effect of EA on the dopaminergic neurons may stem from the collaboration of its anti-inflammatory and neurotrophic actions.
- Published
- 2004
40. Triptolide inhibits TNF-α, IL-1β and NO production in primary microglial cultures
- Author
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Feng-Qiao Li, Xiaomin Wang, Bing Xue, Xian-Yu Liu, Hui-Fang Zhou, Qi-Hua He, Dong-Bin Niu, and Xin-Hong Wang
- Subjects
Male ,Lipopolysaccharide ,medicine.medical_treatment ,Inflammation ,Pharmacology ,Nitric Oxide ,Neuroprotection ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,medicine ,Animals ,Cells, Cultured ,Dose-Response Relationship, Drug ,Microglia ,Tumor Necrosis Factor-alpha ,business.industry ,General Neuroscience ,Phenanthrenes ,Triptolide ,Rats ,medicine.anatomical_structure ,Cytokine ,chemistry ,Immunology ,Epoxy Compounds ,Neuroglia ,Tumor necrosis factor alpha ,Diterpenes ,medicine.symptom ,business ,Interleukin-1 - Abstract
Microglia are believed to participate in the mediation of neurodegeneration through producing a variety of cytotoxic factors upon activation. Pharmacological intervention in microglial activation may therefore exert a neuroprotective effect. In exploring pharmacological agents that can affect microglial activation, we found in this study that triptolide possesses a powerful inhibitory influence over microglia. Pretreatment with triptolide was able to dose-dependently reduce the lipopolysaccharide (LPS)-induced nitrite accumulation and tumor necrosis factor-alpha and interleukin-1beta release from LPS-activated microglia as revealed by Griess reaction and ELISA, respectively. Triptolide reduced LPS-stimulated mRNA expression of all three inflammatory factors. The results obtained from this study demonstrate that triptolide can inhibit inflammatory responses of microglia to inflammatory stimulation via a mechanism involving the inhibition of the synthesis and release of inflammatory factors.
- Published
- 2003
41. Cross-inhibition of NMBR and GRPR signaling maintains normal histaminergic itch transmission
- Author
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Zhou-Feng Chen, Jinbin Xu, Fu-Quan Huo, Zhong Qiu Zhao, Stephanie Krieger, Hui Li, Li Wan, Xian-Yu Liu, Seung Il Kim, Buck E. Rogers, Devin M. Barry, Zhongchun Liu, and Yun-Qing Li
- Subjects
Male ,Nociception ,medicine.medical_specialty ,Neuromedin B receptor ,Biology ,Mice ,Downregulation and upregulation ,Internal medicine ,Gastrin-releasing peptide ,medicine ,Animals ,Receptor ,skin and connective tissue diseases ,Mice, Knockout ,General Neuroscience ,Pruritus ,Histaminergic ,Neural Inhibition ,Articles ,Scratching ,eye diseases ,Mice, Inbred C57BL ,Posterior Horn Cells ,Receptors, Bombesin ,Endocrinology ,Gastrin-Releasing Peptide ,Signal transduction ,Histamine ,Signal Transduction - Abstract
We previously showed that gastrin-releasing peptide receptor (GRPR) in the spinal cord is important for mediating nonhistaminergic itch. Neuromedin B receptor (NMBR), the second member of the mammalian bombesin receptor family, is expressed in a largely nonoverlapping pattern with GRPR in the superficial spinal cord, and its role in itch transmission remains unclear. Here, we report thatNmbrknock-out (KO) mice exhibited normal scratching behavior in response to intradermal injection of pruritogens. However, mice lacking bothNmbrandGrpr(DKO mice) showed significant deficits in histaminergic itch. In contrast, the chloroquine (CQ)-evoked scratching behavior of DKO mice is not further reduced compared withGrprKO mice. These results suggest that NMBR and GRPR could compensate for the loss of each other to maintain normal histamine-evoked itch, whereas GRPR is exclusively required for CQ-evoked scratching behavior. Interestingly, GRPR activity is enhanced inNmbrKO mice despite the lack of upregulation ofGrprexpression; so is NMBR inGrprKO mice. We found that NMB acts exclusively through NMBR for itch transmission, whereas GRP can signal through both receptors, albeit to NMBR to a much lesser extent. Although NMBR and NMBR+neurons are dispensable for histaminergic itch, GRPR+neurons are likely to act downstream of NMBR+neurons to integrate NMB-NMBR-encoded histaminergic itch information in normal physiological conditions. Together, we define the respective function of NMBR and GRPR in itch transmission, and reveal an unexpected relationship not only between the two receptors but also between the two populations of interneurons in itch signaling.
- Published
- 2014
42. Postnatal maintenance of the 5-Ht1a-Pet1 autoregulatory loop by serotonin in the raphe nuclei of the brainstem
- Author
-
Zhou-Feng Chen, Ji-Young Kim, Ana Kim, Xian-Yu Liu, and Zhong Qiu Zhao
- Subjects
medicine.medical_specialty ,Serotonin ,Mouse ,Down-Regulation ,GATA3 Transcription Factor ,Biology ,Tryptophan Hydroxylase ,Development ,Cellular and Molecular Neuroscience ,Mice ,Downregulation and upregulation ,Cell Movement ,Internal medicine ,Tph2 ,polycyclic compounds ,medicine ,Animals ,heterocyclic compounds ,Autoregulatory loop ,Molecular Biology ,Feedback, Physiological ,Mice, Knockout ,TPH2 ,musculoskeletal, neural, and ocular physiology ,Research ,Tryptophan hydroxylase ,Pet1 ,Endocrinology ,nervous system ,Animals, Newborn ,Receptor, Serotonin, 5-HT1A ,Antidepressant ,Raphe Nuclei ,5-HT1A ,Psychopharmacology ,Brainstem ,Raphe nuclei ,Neuroscience ,Serotonergic Neurons ,Transcription Factors - Abstract
Despite the importance of 5-HT1A as a major target for the action of several anxiolytics/antidepressant drugs, little is known about its regulation in central serotonin (5-hydroxytryptamine, 5-HT) neurons. We report that expression of 5-HT1A and the transcription factor Pet1 was impaired in the rostral raphe nuclei of mice lacking tryptophan hydroxylase 2 (Tph2) after birth. The downregulation of Pet1 was recapitulated in 5-Ht1a -/- mice. Using an explant culture system, we show that reduction of Pet1 and 5-HT1A was rescued in Tph2 -/- brainstem by exogenous 5-HT. In contrast, 5-HT failed to rescue reduced expression of Pet1 in 5-Ht1a -/- brainstem explant culture. These results suggest a causal relationship between 5-HT1A and Pet1, and reveal a potential mechanism by which 5-HT1A-Pet1 autoregulatory loop is maintained by 5-HT in a spatiotemporal-specific manner during postnatal development. Our results are relevant to understanding the pathophysiology of certain psychiatric and developmental disorders.
- Published
- 2014
43. Chronic itch development in sensory neurons requires BRAF signaling pathways
- Author
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Zhongchun Liu, Shadmehr Demehri, Joseph Jeffry, Fu-Quan Huo, Ahu Turkoz, Jian Zhong, Li Wan, Zhong Qiu Zhao, Lori L. Hampton, Lynn A. Cornelius, James F. Battey, Zhou-Feng Chen, Xian-Yu Liu, Raphael Kopan, Seung Il Kim, Devin M. Barry, Hui Li, and Kaijie Ma
- Subjects
MAPK/ERK pathway ,Proto-Oncogene Proteins B-raf ,Sensory Receptor Cells ,MAP Kinase Signaling System ,Receptor expression ,TRPV1 ,Gene Expression ,TRPV Cation Channels ,Mice, Transgenic ,Biology ,Receptors, G-Protein-Coupled ,NAV1.8 Voltage-Gated Sodium Channel ,Transient receptor potential channel ,Mice ,otorhinolaryngologic diseases ,Animals ,Humans ,skin and connective tissue diseases ,G protein-coupled receptor ,Mice, Knockout ,Kinase ,Pruritus ,Nociceptors ,General Medicine ,Receptors, Bombesin ,Disease Models, Animal ,Gastrin-Releasing Peptide ,Spinal Cord ,Immunology ,Chronic Disease ,Cancer research ,Nociceptor ,Signal transduction ,Research Article - Abstract
Chronic itch, or pruritus, is associated with a wide range of skin abnormalities. The mechanisms responsible for chronic itch induction and persistence remain unclear. We developed a mouse model in which a constitutively active form of the serine/threonine kinase BRAF was expressed in neurons gated by the sodium channel Nav1.8 (BRAF(Nav1.8) mice). We found that constitutive BRAF pathway activation in BRAF(Nav1.8) mice results in ectopic and enhanced expression of a cohort of itch-sensing genes, including gastrin-releasing peptide (GRP) and MAS-related GPCR member A3 (MRGPRA3), in nociceptors expressing transient receptor potential vanilloid 1 (TRPV1). BRAF(Nav1.8) mice showed de novo neuronal responsiveness to pruritogens, enhanced pruriceptor excitability, and heightened evoked and spontaneous scratching behavior. GRP receptor expression was increased in the spinal cord, indicating augmented coding capacity for itch subsequent to amplified pruriceptive inputs. Enhanced GRP expression and sustained ERK phosphorylation were observed in sensory neurons of mice with allergic contact dermatitis– or dry skin–elicited itch; however, spinal ERK activation was not required for maintaining central sensitization of itch. Inhibition of either BRAF or GRP signaling attenuated itch sensation in chronic itch mouse models. These data uncover RAF/MEK/ERK signaling as a key regulator that confers a subset of nociceptors with pruriceptive properties to initiate and maintain long-lasting itch sensation.
- Published
- 2013
44. Non-canonical Opioid Signaling Inhibits Itch Transmission in the Spinal Cord of Mice.
- Author
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Munanairi, Admire, Xian-Yu Liu, Barry, Devin M., Qianyi Yang, Jun-Bin Yin, Hua Jin, Hui Li, Qing-Tao Meng, Jia-Hang Peng, Zhen-Yu Wu, Jun Yin, Xuan-Yi Zhou, Li Wan, Ping Mo, Seungil Kim, Fu-Quan Huo, Jeffry, Joseph, Yun-Qing Li, Bardoni, Rita, and Bruchas, Michael R.
- Abstract
Chronic itch or pruritus is a debilitating disorder that is refractory to conventional anti-histamine treatment. Kappa opioid receptor (KOR) agonists have been used to treat chronic itch, but the underlying mechanism remains elusive. Here, we find that KOR and gastrin-releasing peptide receptor (GRPR) overlap in the spinal cord, and KOR activation attenuated GRPR-mediated histamine-independent acute and chronic itch in mice. Notably, canonical KOR-mediated Gai signaling is not required for desensitizing GRPR function. In vivo and in vitro studies suggest that KOR activation results in the translocation of Ca2+-independent protein kinase C (PKC)d from the cytosol to the plasma membrane, which in turn phosphorylates and inhibits GRPR activity. A blockade of phospholipase C (PLC) in HEK293 cells prevented KOR-agonist-induced PKCδ translocation and GRPR phosphorylation, suggesting a role of PLC signaling in KOR-mediated GRPR desensitization. These data suggest that a KOR-PLC-PKCδ-GRPR signaling pathway in the spinal cord may underlie KOR-agonists-induced anti-pruritus therapies. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
45. The effect of metformin treatment on endoplasmic reticulum (ER) stress induced by status epilepticus (SE) via the PERK-eIF2α-CHOP pathway.
- Author
-
Jing Chen, Guo Zheng, Hu Guo, Zhong-nan Shi, Jiao Jiang, Xiao-yu Wang, Xiao Yang, and Xian-yu Liu
- Published
- 2018
- Full Text
- View/download PDF
46. Unidirectional cross-activation of GRPR by MOR1D uncouples itch and analgesia induced by opioids
- Author
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Joseph Jeffry, Xian-Yu Liu, Zhou-Feng Chen, Horace H. Loh, Ji-Young Kim, Michael H. Ross, Yan-Gang Sun, Seung Il Kim, Zhongchun Liu, Feng-Fang Tsai, and Qi Fang Li
- Subjects
Gene isoform ,Side effect ,media_common.quotation_subject ,Molecular Sequence Data ,Receptors, Opioid, mu ,Pain ,Pharmacology ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Mice ,otorhinolaryngologic diseases ,medicine ,Animals ,Amino Acid Sequence ,Receptor ,Internalization ,media_common ,Mice, Knockout ,Morphine ,Biochemistry, Genetics and Molecular Biology(all) ,Pruritus ,Scratching ,Analgesics, Opioid ,Receptors, Bombesin ,Opioid ,Signal transduction ,Analgesia ,medicine.drug ,Signal Transduction - Abstract
SummarySpinal opioid-induced itch, a prevalent side effect of pain management, has been proposed to result from pain inhibition. We now report that the μ-opioid receptor (MOR) isoform MOR1D is essential for morphine-induced scratching (MIS), whereas the isoform MOR1 is required only for morphine-induced analgesia (MIA). MOR1D heterodimerizes with gastrin-releasing peptide receptor (GRPR) in the spinal cord, relaying itch information. We show that morphine triggers internalization of both GRPR and MOR1D, whereas GRP specifically triggers GRPR internalization and morphine-independent scratching. Providing potential insight into opioid-induced itch prevention, we demonstrate that molecular and pharmacologic inhibition of PLCβ3 and IP3R3, downstream effectors of GRPR, specifically block MIS but not MIA. In addition, blocking MOR1D-GRPR association attenuates MIS but not MIA. Together, these data suggest that opioid-induced itch is an active process concomitant with but independent of opioid analgesia, occurring via the unidirectional cross-activation of GRPR signaling by MOR1D heterodimerization.
- Published
- 2011
47. Molecular logic circuit based on a multi-state mononuclear platinum(ii) terpyridyl complex
- Author
-
Li-Ping Zhang, Xue Han, Xian-Yu Liu, Chen-Ho Tung, and Li-Zhu Wu
- Subjects
Molecular switch ,Acetylide ,General Physics and Astronomy ,chemistry.chemical_element ,Infrared spectroscopy ,Photochemistry ,Electrochemistry ,chemistry.chemical_compound ,Crystallography ,chemistry ,Ferrocene ,Intramolecular force ,Physical and Theoretical Chemistry ,Platinum ,Metallocene - Abstract
A new type of multi-state platinum(ii) terpyridyl acetylide complex: platinum(ii) 4'-(4-dimethylaminophenyl)-2,2' : 6',2''-terpyridyl ferrocenyl acetylide (1), together with its reference complexes: platinum(ii) 4'-(4-methylphenyl)-2,2' : 6',2''-terpyridyl ferrocenyl acetylide (2), platinum(ii) 4'-(4-dimethylaminophenyl)-2,2' : 6',2''-terpyridyl phenyl acetylide (3) and platinum(ii) 4'-(4-methylphenyl)-2,2' : 6',2''-terpyridyl phenyl acetylide (4), are designed and synthesized. UV-vis-NIR absorption and electrochemical studies demonstrate that complex 1 possesses three ordered intraligand charge transfer (ILCT), ligand-to-ligand charge transfer (LLCT) and metal-to-ligand charge transfer (MLCT) states, and the successive modulation of the intramolecular ILCT, LLCT and MLCT states in a single mononuclear platinum(ii) complex 1 is well evidenced by their reference complexes 2-4. More interestingly, a near-infrared absorption band ranging from 720-1000 nm was clearly observed for complexes 1 and 2 upon oxidation of the σ-bonded ferrocene-ethynyl group by Fe(ClO(4))(3), which was tentatively assigned to platinum(ii)-disturbed ligand-to-metal charge transfer (LM'CT) of the ferrocenium group. These promising features allow us to integrate the multiple states to reproduce basic logic operations at the molecular level. A four-state (LLCT, ILCT, MLCT and LM'CT) molecular switch of complex 1 that responds to the stimulation of H(+), Fe(ClO(4))(3) and Zn producing four outputs has been encoded in binary digits. The logic function executed by complex 1 is equivalent to that of a combinational logic circuit integrating seven or eight logic functions as AND, OR, NOT. A three-input-four-output molecular logic circuit has been established.
- Published
- 2010
48. Regulation of dopamine D3 receptors by protein-protein interactions
- Author
-
Minglei Guo, Limin Mao, John Q. Wang, and Xian-Yu Liu
- Subjects
Physiology ,Biology ,Models, Biological ,Dopamine receptor D3 ,Ca2+/calmodulin-dependent protein kinase ,Enzyme-linked receptor ,Cyclic AMP ,Limbic System ,Animals ,Humans ,5-HT5A receptor ,Protein Interaction Domains and Motifs ,Phosphorylation ,Protein kinase A ,Receptor ,General Neuroscience ,Autophosphorylation ,Receptors, Dopamine D3 ,General Medicine ,Cell biology ,Minireview ,Signal transduction ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,Neuroscience ,Protein Binding ,Signal Transduction - Abstract
Galphai/o protein-coupled dopamine D3 receptors (D3Rs) are preferentially expressed in the limbic system, including the nucleus accumbens. This situates the receptor well in the regulation of limbic function and in the pathogenesis of various neuropsychiatric and neurodegenerative disorders. The intracellular domains of the receptor, mainly the large third intracellular loop and the intracellular C-terminal tail, interact with multiple submembranous proteins. These interactions are critical for the control of surface expression of the receptor and the efficacy of receptor signaling. Recently, a synapse-enriched protein kinase, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), has been found to interact with D3R in the above mentioned interaction model. CaMKII directly binds to the N-terminal of the third loop of D3R. This binding is Ca(2+)-dependent and is sustained by the autophosphorylation of the kinase. In rat accumbal neurons, the increase in Ca(2+) level induces the recruitment of CaMKII to D3R, and CaMKII phosphorylates the receptor at a specific serine site. The CaMKII-induced phosphorylation could inhibit the receptor function and further regulate the behavioral response to the psychostimulant cocaine. These findings reveal a prototypic protein association model between a G protein-coupled receptor and CaMKII. Through the dynamic protein-protein interactions, the abundance, turnover cycle, and function of D3R can be regulated by multiple signals and enzymatic proteins.
- Published
- 2010
49. CaMKIIalpha interacts with M4 muscarinic receptors to control receptor and psychomotor function
- Author
-
John Q. Wang, Xian-Yu Liu, Limin Mao, Minglei Guo, Shilpa Buch, Eugene E. Fibuch, and Eun Sang Choe
- Subjects
medicine.medical_specialty ,Have You Seen...? ,Stimulation ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Cocaine ,Dopamine Uptake Inhibitors ,Dopamine ,Internal medicine ,Ca2+/calmodulin-dependent protein kinase ,Muscarinic acetylcholine receptor ,Protein Interaction Mapping ,medicine ,Animals ,Protein Interaction Domains and Motifs ,Phosphorylation ,Receptor ,Molecular Biology ,Neurons ,Psychomotor function ,General Immunology and Microbiology ,Receptor, Muscarinic M4 ,Kinase ,General Neuroscience ,Corpus Striatum ,Cell biology ,Rats ,Endocrinology ,Calcium ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,Locomotion ,medicine.drug ,Protein Binding - Abstract
Muscarinic acetylcholine receptors (mAChRs) are widely expressed in the mammalian brain and are essential for neuronal functions. These receptors are believed to be actively regulated by intracellular signals, although the underlying mechanisms are largely unknown. In this study, we show that Ca2+/calmodulin‐dependent protein kinase II (CaMKII) binds directly and selectively to one of five mAChR subtypes, M4 receptors (M4Rs), at their C‐terminal regions of second intracellular loops. This binding relies on Ca2+ activation of the kinase and leads to the phosphorylation of M4Rs at a specific threonine site (Thr145). Complementary in vivo studies in rat striatal neurons enriched with M4Rs confirm that rising Ca2+ recruits CaMKIIα to M4Rs to potentiate receptor signalling, which controls behavioural sensitivity to dopamine stimulation in an activity‐dependent manner. Our data identify a new model of protein–protein interactions. In a Ca2+‐sensitive manner, CaMKIIα regulates M4R efficacy and controls the acetylcholine–dopamine balance in the basal ganglia and also the dynamics of movement. There is a [Have you seen ...?][1] (June 2010) associated with this Article. [1]: http://dx.doi.org/10.1038/emboj.2010.105
- Published
- 2010
50. Cellular Basis of Itch Sensation
- Author
-
Xian-Yu Liu, Yan-Gang Sun, Xiu Li Meng, Zhou-Feng Chen, Zhong Qiu Zhao, and Jun Yin
- Subjects
Male ,medicine.medical_specialty ,Spinothalamic tract ,Spinothalamic Tracts ,Central nervous system ,Sensation ,Pain ,Article ,Mice ,Gastrin-releasing peptide ,Internal medicine ,Medicine ,Animals ,Humans ,skin and connective tissue diseases ,Neurons ,Afferent Pathways ,Multidisciplinary ,Behavior, Animal ,business.industry ,Pruritus ,Scratching ,Spinal cord ,Saporins ,Mice, Inbred C57BL ,Receptors, Bombesin ,Endocrinology ,medicine.anatomical_structure ,Spinal Cord ,Chronic Disease ,Ribosome Inactivating Proteins, Type 1 ,Itching ,Bombesin ,Neuron ,medicine.symptom ,business ,Histamine - Abstract
A Separate System for Itch Processing It has been a long-standing question if itch is a subquality of pain involving the same neuronal elements or if distinct, so-called labeled lines exist in the nervous system for both sensations. To address this question directly, Sun et al. (p. 1531 , published online 6 August) destroyed neurons in the superficial spinal dorsal horn that express the gastrin-releasing peptide receptor. This receptor is known to be involved in mediating itch but not pain sensations. In various animal models, ablation of gastrin-releasing peptide receptor-expressing spinal dorsal horn neurons reduced itch without changing pain perception. Thus, itch and pain indeed appear to be mediated by distinct labeled lines in the central nervous system.
- Published
- 2009
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