17 results on '"Huan-jun Lu"'
Search Results
2. Ion channels in cancer-induced bone pain: from molecular mechanisms to clinical applications
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Huan-Jun Lu, Xiao-Bo Wu, and Qian-Qi Wei
- Subjects
chronic pain ,cancer-induced bone pain ,ion channels ,antinociception ,clinical application ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Cancer-induced bone pain (CIBP) caused by bone metastasis is one of the most prevalent diseases, and current treatments rely primarily on opioids, which have significant side effects. However, recent developments in pharmaceutical science have identified several new mechanisms for CIBP, including the targeted modification of certain ion channels and receptors. Ion channels are transmembrane proteins, which are situated on biological cell membranes, which facilitate passive transport of inorganic ions across membranes. They are involved in various physiological processes, including transmission of pain signals in the nervous system. In recent years, there has been an increasing interest in the role of ion channels in chronic pain, including CIBP. Therefore, in this review, we summarize the current literature on ion channels, related receptors, and drugs and explore the mechanism of CIBP. Targeting ion channels and regulating their activity might be key to treating pain associated with bone cancer and offer new treatment avenues.
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- 2023
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3. Evaluation of the Anti-Inflammatory Pain Effect of Ginsenoside-Conjugated O-Carboxymethyl Chitosan Particles
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Huan-Jun Lu, Jian-Ke Cen, Yu Ren, and Mei-Xian Li
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O-carboxymethyl chitosan ,ginsenoside Rh2 ,anti-nociception ,inflammatory pain ,Organic chemistry ,QD241-441 - Abstract
Nanoparticle delivery of functional molecules or vaccines is an effective method for the treatment of many diseases. This study aims to design ginsenoside Rh2-conjugated O-carboxymethyl chitosan (O-CMC/Rh2) as a drug delivery system and explore its anti-nociceptive effects. O-CMC/Rh2 was synthesized with an esterification reaction, and its chemical composition and morphology were evaluated using proton nuclear magnetic resonance (1H NMR), the attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy, and scanning electron microscopy (SEM). In addition, the in vitro cumulative release of Rh2 from the O-CMC/Rh2 was also evaluated under different pH conditions. The results showed that the ginsenoside Rh2 was successfully conjugated to the O-CMC matrix and exhibited a highly porous structure after conjugation, facilitating the release of Rh2 from O-CMC. Complete Freund’s adjuvant (CFA) and burn injury-induced pain models were used to evaluate the anti-nociceptive effects of O-CMC/Rh2 on inflammatory pain. O-CMC/Rh2 reduced CFA-induced pain hypersensitivity in a dose-dependent manner and had a longer analgesic effect than Rh2. In addition, O-CMC/Rh2 also relieved the chronic pain induced by bury injury. These results indicated that O-CMC/Rh2 could be useful in reducing inflammatory pain, thus possessing a potential medicinal application in pain therapy.
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- 2023
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4. Correction: Challenges and advances in materials and fabrication technologies of small-diameter vascular grafts
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Mei-Xian Li, Qian-Qi Wei, Hui-Lin Mo, Yu Ren, Wei Zhang, Huan-Jun Lu, and Yoon Ki Joung
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Medical technology ,R855-855.5 - Published
- 2023
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5. Progress on the Elucidation of the Antinociceptive Effect of Ginseng and Ginsenosides in Chronic Pain
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Mei-Xian Li, Qian-Qi Wei, and Huan-Jun Lu
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chronic pain ,ginseng ,ginsenosides ,antinociception ,anti-inflammation ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Ginseng (Panax ginseng C.A. Meyer) is a traditional Oriental herbal drug widely used in East Asia. Its main active ingredients are ginsenosides whose constituents are known to have various pharmacological activities such as anticancer, antinociception, and neuroprotection. The analgesic effects of ginsenosides, such as Rg1, Rg2, and Rb1, as well as compound K, are well known and the analgesic mechanism of action in inflammatory pain models is thought to be the down regulation of pro-inflammatory cytokine expression (TNF-α IL-1β, and IL-6). Several studies have also demonstrated that ginsenosides regulate neuropathic pain through the modulation of estrogen receptors. Recently, an increasing number of pathways have emerged in relation to the antinociceptive effect of ginseng and ginsenosides. Therefore, this review presents our current understanding of the effectiveness of ginseng in chronic pain and how its active constituents regulate nociceptive responses and their mechanisms of action.
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- 2022
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6. Neuroinflammation in HIV-Related Neuropathic Pain
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Huan-Jun Lu, Yuan-Yuan Fu, Qian-Qi Wei, and Zhi-Jun Zhang
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neuroinfalmmation ,Chemokine ,HIV ,Human immunodeficiency virus ,microglia ,neuropathic pain (NP) ,Therapeutics. Pharmacology ,RM1-950 - Abstract
In the management of human immunodeficiency virus (HIV) infection around the world, chronic complications are becoming a new problem along with the prolonged life expectancy. Chronic pain is widespread in HIV infected patients and even affects those with a low viral load undergoing long-term treatment with antiviral drugs, negatively influencing the adherence to disease management and quality of life. A large proportion of chronic pain is neuropathic pain, which defined as chronic pain caused by nervous system lesions or diseases, presenting a series of nervous system symptoms including both positive and negative signs. Injury caused by HIV protein, central and peripheral sensitization, and side effects of antiretroviral therapy lead to neuroinflammation, which is regarded as a maladaptive mechanism originally serving to promote regeneration and healing, constituting the main mechanism of HIV-related neuropathic pain. Gp120, as HIV envelope protein, has been found to be the major toxin that induces neuropathic pain. Particularly, the microglia, releasing numerous pro-inflammatory substances (such as TNFα, IL-1β, and IL-6), not only sensitize the neurons but also are the center part of the crosstalk bridging the astrocytes and oligodendrocytes together forming the central sensitization during HIV infection, which is not discussed detailly in recent reviews. In the meantime, some NRTIs and PIs exacerbate the neuroinflammation response. In this review, we highlight the importance of clarifying the mechanism of HIV-related neuropathic pain, and discuss about the limitation of the related studies as future research directions.
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- 2021
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7. Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia.
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Huan-Jun Lu, Daji Guo, and Qian-Qi Wei
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NEUROINFLAMMATION , *TUBERCULOUS meningitis , *MICROGLIA - Abstract
Tuberculous meningitis (TBM) is the most severe complication of tuberculosis (TB) and is associated with high rates of disability and mortality. Mycobacterium tuberculosis (M. tb), the infectious agent of TB, disseminates from the respiratory epithelium, breaks through the blood-brain barrier, and establishes a primary infection in the meninges. Microglia are the core of the immune network in the central nervous system (CNS) and interact with glial cells and neurons to fight against harmful pathogens and maintain homeostasis in the brain through pleiotropic functions. However, M. tb directly infects microglia and resides in them as the primary host for bacillus infections. Largely, microglial activation slows disease progression. The non-productive inflammatory response that initiates the secretion of pro-inflammatory cytokines and chemokines may be neurotoxic and aggravate tissue injuries based on damages caused by M. tb. Host-directed therapy (HDT) is an emerging strategy for modulating host immune responses against diverse diseases. Recent studies have shown that HDT can control neuroinflammation in TBM and act as an adjunct therapy to antibiotic treatment. In this review, we discuss the diverse roles of microglia in TBM and potential host-directed TB therapies that target microglia to treat TBM. We also discuss the limitations of applying each HDT and suggest a course of action for the near future. [ABSTRACT FROM AUTHOR]
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- 2024
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8. The Shackling Effect in Cyclic Azobenzene Liquid Crystal
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Huan-jun Lu, Xiao-Hong Li, Zi-Fan Yang, Er-Qiang Chen, and Ying-Feng Tu, Yang Xiao, and Chong He
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chemistry.chemical_classification ,Phase transition ,Materials science ,Polymers and Plastics ,General Chemical Engineering ,Dimer ,Organic Chemistry ,Polymer ,Isothermal process ,chemistry.chemical_compound ,Crystallography ,chemistry ,Azobenzene ,Liquid crystal ,Phase (matter) ,Isomerization - Abstract
We demonstrate here a novel method for the design of liquid crystals (LCs) via the cyclization of mesogens by flexible chains. For two azobenzene-4,4’-dicarboxylate derivatives, the cyclic dimer, cyclic bis(tetraethylene glycol azobenzene-4,4′-dicarboxylate) (CBTAD), shows LC properties with smectic A phase, while its linear counterpart, bis(2-(2’-hydroxyethyloxy)ethyl azobenzene-4,4′-dicarboxylate (BHAD), has no LC phase. The difference is ascribed to the shackling effect from the cyclic topology, which leads to the much smaller entropy change during phase transitions and increases the isotropic temperature greatly for cyclics. In addition, the trans-to-cis isomerization of azobenzene groups under UV-light is also limited in CBTAD. With the reversible isomerization of azobenzene groups, CBTAD showed interesting isothermal phase transition behaviors, where the LC phase disappeared upon photoirradiation of 365 nm UV-light, and recovered when the UV-light was off. Combined with the smectic LC nature, a novel UV-light tuned visible light regulator was designed, by simply placing CBTAD in two glass plates. The scattered phase of smectic LC was utilized as the “OFF” state for light passage, while the UV-light induced isotropic phase was utilized as the “ON” state. The shackling effect outlined here should be applicable for the design of cyclic LC oligomers/polymers with special properties.
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- 2022
9. Anoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor–dependent itch
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Hyesu Kim, Hyungsup Kim, Hawon Cho, Byeongjun Lee, Huan-Jun Lu, Kyungmin Kim, Sooyoung Chung, Won-Sik Shim, Young Kee Shin, Xinzhong Dong, John N. Wood, and Uhtaek Oh
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Mice ,Anesthesiology and Pain Medicine ,Neurology ,Chloride Channels ,GTP-Binding Proteins ,Ganglia, Spinal ,Pruritus ,Animals ,Chloroquine ,Neurology (clinical) ,Anoctamin-1 - Abstract
Itch is an unpleasant sensation that evokes a desire to scratch. Pathologic conditions such as allergy or atopic dermatitis produce severe itching sensation. Mas-related G protein receptors (Mrgprs) are receptors for many endogenous pruritogens. However, signaling pathways downstream to these receptors in dorsal root ganglion (DRG) neurons are not yet understood. We found that anoctamin 1 (ANO1), a Ca 2+ -activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of Ano1 in DRG neurons displayed a significant reduction in scratching behaviors in response to acute and chronic Mrgpr-dependent itch models and the epidermal hyperplasia induced by dry skin. In vivo Ca 2+ imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of Ano1 in DRG neurons of Ano1 -deficient mice rescued the impaired itching observed in Ano1 -deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.
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- 2022
10. Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia
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Qian-Qi Wei, Daji Guo, and Huan-Jun Lu
- Subjects
Cell Biology ,Neurology (clinical) ,Geriatrics and Gerontology ,Pathology and Forensic Medicine - Published
- 2023
11. Ginsenoside Rh2 Ameliorates Neuropathic Pain by inhibition of the miRNA21-TLR8-mitogen-activated protein kinase axis
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Yuan-Yuan Fu, Jian-Ke Cen, Hao-Lin Song, Si-Yuan Song, Zhi-Jun Zhang, and Huan-Jun Lu
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Analgesics ,Ginsenosides ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,Anti-Inflammatory Agents ,Ligands ,Rats ,Rats, Sprague-Dawley ,Cellular and Molecular Neuroscience ,Mice ,MicroRNAs ,Anesthesiology and Pain Medicine ,Neuroprotective Agents ,Hyperalgesia ,Toll-Like Receptor 8 ,Molecular Medicine ,Animals ,Neuralgia ,Extracellular Signal-Regulated MAP Kinases - Abstract
Ginsenoside Rh2 is one of the major bioactive ginsenosides in Panax ginseng. Although Rh2 is known to enhance immune cells activity for treatment of cancer, its anti-inflammatory and neuroprotective effects have yet to be determined. In this study, we investigated the effects of Rh2 on spared nerve injury (SNI)-induced neuropathic pain and elucidated the potential mechanisms. We found that various doses of Rh2 intrathecal injection dose-dependently attenuated SNI-induced mechanical allodynia and thermal hyperalgesia. Rh2 also inhibited microglia and astrocyte activation in the spinal cord of a murine SNI model. Rh2 treatment inhibited SNI-induced increase of proinflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1 and IL-6. Expression of miRNA-21, an endogenous ligand of Toll like receptor (TLR)8 was also decreased. Rh2 treatment blocked the mitogen-activated protein kinase (MAPK) signaling pathway by inhibiting of phosphorylated extracellular signal-regulated kinase expression. Finally, intrathecal injection of TLR8 agonist VTX-2337 reversed the analgesic effect of Rh2. These results indicated that Rh2 relieved SNI-induced neuropathic pain via inhibiting the miRNA-21-TLR8-MAPK signaling pathway, thus providing a potential application of Rh2 in pain therapy.
- Published
- 2022
12. β-adrenergic Receptor Activity in the Hippocampal Dentate Gyrus Participates in Spatial Learning and Memory Impairment in Sleep-deprived Rats
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Huan-Jun Lu and Jing lv
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Receptor expression ,Morris water navigation task ,AMPA receptor ,Hippocampal formation ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Internal medicine ,medicine ,Spatial learning and memory ,Chemistry ,Dentate gyrus ,Long-term potentiation ,β-adrenoceptors ,Sleep deprivation ,030104 developmental biology ,Endocrinology ,Excitatory postsynaptic potential ,NMDA receptor ,Original Article ,Hippocampal dentate gyrus ,Neurology (clinical) ,030217 neurology & neurosurgery - Abstract
Sleep deprivation (SD) leads to cognitive impairment, especially hippocampus-dependent learning and memory (L&M). The hippocampal dentate gyrus (DG) is the key structure involved in spatial L&M while long-term potentiation (LTP) is an important cellular mechanism responsible for L&M. Physiological and behavioral evidences support the hypothesis that norepinephrine (NE) and β-adrenoceptors (β-AR) may play an important role in regulating L&M, including LTP. However, it is enigmatic how β-AR influences the LTP disruption or memory impairment under SD circumstances. In the present study, the rats were subjected to SD for 18 h per day for 21 consecutive days and cognitive capacity was assessed by the Morris water maze (MWM) test. We examined the extracellular concentration of NE in the DG using in vivo brain microdialysis and HPLC analysis. The amplitudes of field excitatory postsynaptic potential (fEPSP) were subsequently measured in the DG during MWM test in freely moving conscious rats. The extracellular concentrations of NE and fEPSP amplitudes in the DG were significantly increased during MWM test, while these responses were suppressed in SD rats. When fEPSP amplitudes in the DG were measured after local injection of isoproterenol (an agonist of β-AR), SD rats significantly alleviated the fEPSP impairment and rescued deficits of spatial L&M. In addition, the reduced expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in SD rats significantly increased by activation of β-AR by isoproterenol in the DG. In conclusion, we propose that β-adrenergic signaling can improve memory impairment in sleep-deficient rats by regulating synaptic efficiency and glutamatergic receptor expression.
- Published
- 2021
13. Enhanced function of NR2C/2D-containing NMDA receptor in the nucleus accumbens contributes to peripheral nerve injury-induced neuropathic pain and depression in mice
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Peng-Bo Jing, Xiao-Hong Chen, Huan-Jun Lu, Yong-Jing Gao, and Xiao-Bo Wu
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neuropathic pain ,Depression ,musculoskeletal, neural, and ocular physiology ,Short Report ,NR2C ,NR2D ,NMDA receptor ,Receptors, N-Methyl-D-Aspartate ,Nucleus Accumbens ,Cellular and Molecular Neuroscience ,Mice ,Anesthesiology and Pain Medicine ,nervous system ,Peripheral Nerve Injuries ,Molecular Medicine ,Animals ,Humans ,Neuralgia - Abstract
N-methyl-d-aspartate receptors (NMDARs) dysfunction in the nucleus accumbens (NAc) participates in regulating many neurological and psychiatric disorders such as drug addiction, chronic pain, and depression. NMDARs are heterotetrameric complexes generally composed of two NR1 and two NR2 subunits (NR2A, NR2B, NR2C and NR2D). Much attention has been focused on the role of NR2A and NR2B-containing NMDARs in a variety of neurological disorders; however, the function of NR2C/2D subunits at NAc in chronic pain remains unknown. In this study, spinal nerve ligation (SNL) induced a persistent sensory abnormity and depressive-like behavior. The whole-cell patch clamp recording on medium spiny neurons (MSNs) in the NAc showed that the amplitude of NMDAR-mediated excitatory postsynaptic currents (EPSCs) was significantly increased when membrane potential held at −40 to 0 mV in mice after 14 days of SNL operation. In addition, selective inhibition of NR2C/2D-containing NMDARs with PPDA caused a larger decrease on peak amplitude of NMDAR-EPSCs in SNL than that in sham-operated mice. Appling of selective potentiator of NR2C/2D, CIQ, markedly enhanced the evoked NMDAR-EPSCs in SNL-operated mice, but no change in sham-operated mice. Finally, intra-NAc injection of PPDA significantly attenuated SNL-induced mechanical allodynia and depressive-like behavior. These results for the first time showed that the functional change of NR2C/2D subunits-containing NMDARs in the NAc might contribute to the sensory and affective components in neuropathic pain.
- Published
- 2022
14. Tentonin 3/TMEM150C senses blood pressure changes in the aortic arch.
- Author
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Huan-Jun Lu, Thien-Luan Nguyen, Gyu-Sang Hong, Sungmin Pak, Hyesu Kim, Hyungsup Kim, Dong-Yoon Kim, Sung-Yon Kim, Yiming Shen, Pan Dong Ryu, Mi-Ock Lee, Uhtaek Oh, Lu, Huan-Jun, Nguyen, Thien-Luan, Hong, Gyu-Sang, Pak, Sungmin, Kim, Hyesu, Kim, Hyungsup, Kim, Dong-Yoon, and Kim, Sung-Yon
- Abstract
The baroreceptor reflex is a powerful neural feedback that regulates arterial pressure (AP). Mechanosensitive channels transduce pulsatile AP to electrical signals in baroreceptors. Here we show that tentonin 3 (TTN3/TMEM150C), a cation channel activated by mechanical strokes, is essential for detecting AP changes in the aortic arch. TTN3 was expressed in nerve terminals in the aortic arch and nodose ganglion (NG) neurons. Genetic ablation of Ttn3 induced ambient hypertension, tachycardia, AP fluctuations, and impaired baroreflex sensitivity. Chemogenetic silencing or activation of Ttn3+ neurons in the NG resulted in an increase in AP and heart rate, or vice versa. More important, overexpression of Ttn3 in the NG of Ttn3-/- mice reversed the cardiovascular changes observed in Ttn3-/- mice. We conclude that TTN3 is a molecular component contributing to the sensing of dynamic AP changes in baroreceptors. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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15. Analysis of the Baroreceptor and Vestibular Receptor Inputs in the Rostral Ventrolateral Medulla following Hypotension in Conscious Rats
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Xian Jiang, Joo Young Park, Yan Lan, Byung Rim Park, Yuan-Zhe Jin, Huan-Jun Lu, Min Sun Kim, Guang-Shi Jin, Li-Wei Li, and Yan-Zhao Yang
- Subjects
Pharmacology ,Vestibular system ,endocrine system ,medicine.medical_specialty ,Baroreceptor ,Physiology ,business.industry ,Vestibular receptor ,Glutamate receptor ,Rostral ventrolateral medulla ,Endocrinology ,Blood pressure ,Anesthesia ,Internal medicine ,medicine ,Extracellular ,Original Article ,Sodium nitroprusside ,Hypotension ,Receptor ,business ,medicine.drug - Abstract
Input signals originating from baroreceptors and vestibular receptors are integrated in the rostral ventrolateral medulla (RVLM) to maintain blood pressure during postural movement. The contribution of baroreceptors and vestibular receptors in the maintenance of blood pressure following hypotension were quantitatively analyzed by measuring phosphorylated extracellular regulated protein kinase (pERK) expression and glutamate release in the RVLM. The expression of pERK and glutamate release in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) following hypotension induced by a sodium nitroprusside (SNP) infusion. The expression of pERK was significantly increased in the RVLM in the control group following SNP infusion, and expression peaked 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than seen in the control group. The SAD group showed a relatively higher reduction in pERK expression when compared with the BL group. The level of glutamate release was significantly increased in the RVLM in control, BL, SAD groups following SNP infusion, and this peaked 10 min after SNP infusion. The SAD group showed a relatively higher reduction in glutamate release when compared with the BL group. These results suggest that the baroreceptors are more powerful in pERK expression and glutamate release in the RVLM following hypotension than the vestibular receptors, but the vestibular receptors still have an important role in the RVLM.
- Published
- 2015
16. Functional Connections of the Vestibulo-spino-adrenal Axis in the Control of Blood Pressure Via the Vestibulosympathetic Reflex in Conscious Rats
- Author
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Huan Jun Lu, Yuan-Zhe Jin, Byung Rim Park, Sang Eon Park, Mei Zhi Li, Min Sun Kim, and Mei Han Li
- Subjects
Pharmacology ,medicine.medical_specialty ,Epinephrine ,Intermediolateral cell column ,Vestibulo-spino-adrenal axis ,Physiology ,business.industry ,Medial vestibular nucleus ,c-Fos protein ,Rostral ventrolateral medulla ,AMPA receptor ,Vestibulosympathetic reflex ,chemistry.chemical_compound ,Endocrinology ,Blood pressure ,chemistry ,Internal medicine ,medicine ,Reflex ,CNQX ,NMDA receptor ,Original Article ,Glutamate ,business ,Microinjection - Abstract
Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements. In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation. Expression of c-Fos protein in the intermediolateral cell column of the middle thoracic spinal regions and blood epinephrine levels were investigated, following microinjection of glutamate receptor agonists or antagonists into the medial vestibular nucleus (MVN) and/or sodium nitroprusside (SNP)-induced hypotension. Both microinjection of glutamate receptor agonists (NMDA and AMPA) into the MVN or rostral ventrolateral medullary nucleus (RVLM) and SNP-induced hypotension led to increased number of c-Fos positive neurons in the intermediolateral cell column of the middle thoracic spinal regions and increased blood epinephrine levels. Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels. These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.
- Published
- 2015
17. Analysis of the Baroreceptor and Vestibular Receptor Inputs in the Rostral Ventrolateral Medulla following Hypotension in Conscious Rats.
- Author
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Yan Lan, Huan-Jun Lu, Xian Jiang, Li-Wei Li, Yan-Zhao Yang, Guang-Shi Jin, Joo Young Park, Min Sun Kim, Byung Rim Park, and Yuan-Zhe Jin
- Subjects
- *
BARORECEPTORS , *HYPOTENSION , *LABORATORY rats , *BLOOD pressure , *EXTRACELLULAR signal-regulated kinases , *PROTEIN expression - Abstract
Input signals originating from baroreceptors and vestibular receptors are integrated in the rostral ventrolateral medulla (RVLM) to maintain blood pressure during postural movement. The contribution of baroreceptors and vestibular receptors in the maintenance of blood pressure following hypotension were quantitatively analyzed by measuring phosphorylated extracellular regulated protein kinase (pERK) expression and glutamate release in the RVLM. The expression of pERK and glutamate release in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) following hypotension induced by a sodium nitroprusside (SNP) infusion. The expression of pERK was significantly increased in the RVLM in the control group following SNP infusion, and expression peaked 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than seen in the control group. The SAD group showed a relatively higher reduction in pERK expression when compared with the BL group. The level of glutamate release was significantly increased in the RVLM in control, BL, SAD groups following SNP infusion, and this peaked 10 min after SNP infusion. The SAD group showed a relatively higher reduction in glutamate release when compared with the BL group. These results suggest that the baroreceptors are more powerful in pERK expression and glutamate release in the RVLM following hypotension than the vestibular receptors, but the vestibular receptors still have an important role in the RVLM. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
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