16 results on '"Gemma Gou"'
Search Results
2. Endogenous Syngap1 alpha splice forms promote cognitive function and seizure protection
- Author
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Murat Kilinc, Vineet Arora, Thomas K Creson, Camilo Rojas, Aliza A Le, Julie Lauterborn, Brent Wilkinson, Nicolas Hartel, Nicholas Graham, Adrian Reich, Gemma Gou, Yoichi Araki, Àlex Bayés, Marcelo Coba, Gary Lynch, Courtney A Miller, and Gavin Rumbaugh
- Subjects
Syngap1 ,splicing ,isoforms ,cognition ,behavior ,seizure ,Medicine ,Science ,Biology (General) ,QH301-705.5 - Abstract
Loss-of-function variants in SYNGAP1 cause a developmental encephalopathy defined by cognitive impairment, autistic features, and epilepsy. SYNGAP1 splicing leads to expression of distinct functional protein isoforms. Splicing imparts multiple cellular functions of SynGAP proteins through coding of distinct C-terminal motifs. However, it remains unknown how these different splice sequences function in vivo to regulate neuronal function and behavior. Reduced expression of SynGAP-α1/2 C-terminal splice variants in mice caused severe phenotypes, including reduced survival, impaired learning, and reduced seizure latency. In contrast, upregulation of α1/2 expression improved learning and increased seizure latency. Mice expressing α1-specific mutations, which disrupted SynGAP cellular functions without altering protein expression, promoted seizure, disrupted synapse plasticity, and impaired learning. These findings demonstrate that endogenous SynGAP isoforms with α1/2 spliced sequences promote cognitive function and impart seizure protection. Regulation of SynGAP-αexpression or function may be a viable therapeutic strategy to broadly improve cognitive function and mitigate seizure.
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- 2022
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3. Evolution of complexity in the zebrafish synapse proteome
- Author
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Àlex Bayés, Mark O. Collins, Rita Reig-Viader, Gemma Gou, David Goulding, Abril Izquierdo, Jyoti S. Choudhary, Richard D. Emes, and Seth G. N. Grant
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Science - Abstract
Systematic analysis of the zebrafish synapse proteome has been lacking. Here the authors characterize the ultrastructure of zebrafish synapse and compare the proteomes of postsynaptic density in zebrafish and mice, offering a resource for future studies using zebrafish to model diseases.
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- 2017
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4. Design, optimization and validation of genes commonly used in expression studies on DMH/AOM rat colon carcinogenesis model
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David Bars-Cortina, Antoni Riera-Escamilla, Gemma Gou, Carme Piñol-Felis, and María-José Motilva
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qPCR ,Dimethylhydrazine (DMH) ,Azoxymethane (AOM) ,Colon ,SYBR ,Gene validation ,Medicine ,Biology (General) ,QH301-705.5 - Abstract
Colorectal cancer (CRC), also known as colon cancer, is the third most common form of cancer worldwide in men and the second in women and is characterized by several genetic alterations, among them the expression of several genes. 1,2-dimethylhydrazine (DMH) and its metabolite azoxymethane (AOM) are procarcinogens commonly used to induce colon cancer in rats (DMH/AOM rat model). This rat model has been used to study changes in mRNA expression in genes involved in this pathological condition. However, a lack of proper detailed PCR primer design in the literature limits the reproducibility of the published data. The present study aims to design, optimize and validate the qPCR, in accordance with the MIQE (Minimum Information for Publication of Quantitative Real-Time PCR Experiments) guidelines, for seventeen genes commonly used in the DMH/AOM rat model of CRC (Apc, Aurka, Bax, Bcl2, β-catenin, Ccnd1, Cdkn1a, Cox2, Gsk3beta, IL-33, iNOs, Nrf2, p53, RelA, Smad4, Tnfα and Vegfa) and two reference genes (Actb or β-actin and B2m). The specificity of all primer pairs was empirically validated on agarose gel, and furthermore, the melting curve inspection was checked as was their efficiency (%) ranging from 90 to 110 with a correlation coefficient of r2 > 0.980. Finally, a pilot study was performed to compare the robustness of two candidate reference genes.
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- 2019
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5. Metazoan evolution of glutamate receptors reveals unreported phylogenetic groups and divergent lineage-specific events
- Author
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David Ramos-Vicente, Jie Ji, Esther Gratacòs-Batlle, Gemma Gou, Rita Reig-Viader, Javier Luís, Demian Burguera, Enrique Navas-Perez, Jordi García-Fernández, Pablo Fuentes-Prior, Hector Escriva, Nerea Roher, David Soto, and Àlex Bayés
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phylogenetics ,ionotropic glutamate receptors ,metabotropic glutamate receptors ,electrophysiology ,gene expression ,amphioxus ,Medicine ,Science ,Biology (General) ,QH301-705.5 - Abstract
Glutamate receptors are divided in two unrelated families: ionotropic (iGluR), driving synaptic transmission, and metabotropic (mGluR), which modulate synaptic strength. The present classification of GluRs is based on vertebrate proteins and has remained unchanged for over two decades. Here we report an exhaustive phylogenetic study of GluRs in metazoans. Importantly, we demonstrate that GluRs have followed different evolutionary histories in separated animal lineages. Our analysis reveals that the present organization of iGluRs into six classes does not capture the full complexity of their evolution. Instead, we propose an organization into four subfamilies and ten classes, four of which have never been previously described. Furthermore, we report a sister class to mGluR classes I-III, class IV. We show that many unreported proteins are expressed in the nervous system, and that new Epsilon receptors form functional ligand-gated ion channels. We propose an updated classification of glutamate receptors that includes our findings.
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- 2018
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6. Author response: Endogenous Syngap1 alpha splice forms promote cognitive function and seizure protection
- Author
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Murat Kilinc, Vineet Arora, Thomas K Creson, Camilo Rojas, Aliza A Le, Julie Lauterborn, Brent Wilkinson, Nicolas Hartel, Nicholas Graham, Adrian Reich, Gemma Gou, Yoichi Araki, Àlex Bayés, Marcelo Coba, Gary Lynch, Courtney A Miller, and Gavin Rumbaugh
- Published
- 2022
7. Endogenous Syngap1 Alpha Splice Forms Promote Cognitive Function and Seizure Protection
- Author
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Murat Kilinc, Vineet Arora, Thomas K Creson, Camilo Rojas, Aliza A Le, Julie Lauterborn, Brent Wilkinson, Nicolas Hartel, Nicholas Graham, Adrian Reich, Gemma Gou, Yoichi Araki, Àlex Bayés, Marcelo Coba, Gary Lynch, Courtney A Miller, and Gavin Rumbaugh
- Subjects
General Immunology and Microbiology ,General Neuroscience ,General Medicine ,General Biochemistry, Genetics and Molecular Biology - Abstract
SummaryLoss-of-function variants in SYNAGP1 cause a developmental encephalopathy defined by cognitive impairment, autistic features, and epilepsy. SYNGAP1 splicing leads to expression of distinct functional protein isoforms. Splicing imparts multiple cellular functions of SynGAP proteins through coding of distinct C-terminal motifs. However, it remains unknown how these different splice sequences function in vivo to regulate neuronal function and behavior. Reduced expression of SynGAP-α1/2 C-terminal splice variants in mice caused severe phenotypes, including reduced survival, impaired learning, and reduced seizure latency. In contrast, upregulation of α1/2 expression improved learning and increased seizure latency. Mice expressing α1-specific mutations, which disrupted SynGAP cellular functions without altering protein expression, promoted seizure, disrupted synapse plasticity, and impaired learning. These findings demonstrate that endogenous SynGAP isoforms with α1/2 spliced sequences promote cognitive function and impart seizure protection. Regulation of SynGAP-α expression or function may be a viable therapeutic strategy to broadly improve cognitive function and mitigate seizure.
- Published
- 2021
8. Endogenous
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Murat, Kilinc, Vineet, Arora, Thomas K, Creson, Camilo, Rojas, Aliza A, Le, Julie, Lauterborn, Brent, Wilkinson, Nicolas, Hartel, Nicholas, Graham, Adrian, Reich, Gemma, Gou, Yoichi, Araki, Àlex, Bayés, Marcelo, Coba, Gary, Lynch, Courtney A, Miller, and Gavin, Rumbaugh
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Mice ,Cognition ,Seizures ,ras GTPase-Activating Proteins ,Mutation ,Synapses ,Animals ,Protein Isoforms - Abstract
Loss-of-function variants in
- Published
- 2021
9. Splicing of the SynGAP Carboxyl-Terminus Enables Isoform-Specific Tuning of NMDA Receptor Signaling Linked to Cognitive Function
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Gemma Gou, Courtney A. Miller, Murat Kilinc, Nicholas A. Graham, Sabyasachi Maity, Gavin Rumbaugh, Yoichi Araki, Adrian Reich, Brent Wilkinson, Nicolas G. Hartel, Julie C. Lauterborn, Camilo Rojas, Aliza A. Le, Thomas K. Creson, Marcelo P. Coba, Gary Lynch, and Àlex Bayés
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0303 health sciences ,Chemistry ,PDZ domain ,fungi ,Long-term potentiation ,chemical and pharmacologic phenomena ,SYNGAP1 ,Postsynaptic density organization ,Synapse ,03 medical and health sciences ,0302 clinical medicine ,Excitatory postsynaptic potential ,NMDA receptor ,Synaptic signaling ,Neuroscience ,030217 neurology & neurosurgery ,030304 developmental biology - Abstract
SummarySynGAP-α1 is a splice variant of the neurodevelopmental disorder risk gene, SYNGAP1/Syngap1. α1 encodes the C-terminal PDZ binding motif (PBM) that promotes liquid-liquid phase separation, a candidate process for postsynaptic density organization within excitatory synapses. However, it remains unknown how the endogenous SynGAP PBM regulates synapse properties and related cognitive functions. We found that a major PBM function in mice is to limit the mobility of SynGAP-α1 in response to NMDA receptor activation. Genetic disruption of the PBM increased SynGAP-α1 mobility to levels consistent with other non-PBM-containing C-terminal isoforms. This resulted in a lowering of the threshold for NMDA receptor-dependent signaling required for plasticity, leading to aberrant strengthening of excitatory synapses in spontaneously active neurons. PBM-deficient animals also exhibited a lower seizure threshold, disrupted LTP, and impaired cognition. Thus, the PBM enables isoform-specific SynGAP gating of NMDA receptor function, a mechanism linking synaptic signaling dynamics to network excitability and cognition.
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- 2020
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10. SynGAP Splice Variants Display Heterogeneous Spatio-Temporal Expression And Subcellular Distribution In The Developing Mammalian Brain
- Author
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Richard L. Huganir, Cristian de Quintana-Schmidt, Murat Kilinc, Àlex Bayés, Gavin Rumbaugh, Yoichi Araki, Elena Serrano, Adriana Roca-Fernandez, Gemma Gou, and Rita Reig-Viader
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Proteomics ,0301 basic medicine ,Gene isoform ,SynGAP ,Hippocampus ,GTPase ,Biology ,Biochemistry ,Synapse ,Mice ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Isomerism ,Postsynaptic potential ,pleiotropy ,subcellular localization ,Animals ,Humans ,Protein Isoforms ,Computer Simulation ,Cerebral Cortex ,Brain ,Gene Expression Regulation, Developmental ,Signal Transduction & Synaptic Transmission ,Subcellular localization ,Cell biology ,Mice, Inbred C57BL ,postnatal development ,protein expression pattern ,030104 developmental biology ,ras GTPase-Activating Proteins ,Forebrain ,Original Article ,protein isoforms ,Signal transduction ,ORIGINAL ARTICLES ,Postsynaptic density ,030217 neurology & neurosurgery ,Subcellular Fractions - Abstract
The SynGAP protein is a major regulator of synapse biology and neural circuit function. Genetic variants linked to epilepsy and intellectual disability disrupt synaptic function and neural excitability. SynGAP has been involved in multiple signaling pathways and can regulate small GTPases with very different roles. Yet, the molecular bases behind this pleiotropy are poorly understood. We hypothesize that different SynGAP isoforms will mediate different sets of functions and that deciphering their spatio‐temporal expression and subcellular localization will accelerate understanding their multiple functions. Using isoform‐specific antibodies recognizing SynGAP in mouse and human samples we found distinctive developmental expression patterns for all SynGAP isoforms in five mouse brain areas. Particularly noticeable was the delayed expression of SynGAP‐α1 isoforms, which directly bind to postsynaptic density‐95, in cortex and hippocampus during the first 2 weeks of postnatal development. Suggesting that during this period other isoforms would have a more prominent role. Furthermore, we observed subcellular localization differences between isoforms, particularly throughout postnatal development. Consistent with previous reports, SynGAP was enriched in the postsynaptic density in the mature forebrain. However, SynGAP was predominantly found in non‐synaptic locations in a period of early postnatal development highly sensitive to SynGAP levels. While, α1 isoforms were always found enriched in the postsynaptic density, α2 isoforms changed from a non‐synaptic to a mostly postsynaptic density localization with age and β isoforms were always found enriched in non‐synaptic locations. The differential expression and subcellular distribution of SynGAP isoforms may contribute to isoform‐specific regulation of small GTPases, explaining SynGAP pleiotropy., Syngap1 gene encodes for different synaptic Ras/Rap GTPase‐activating (SynGAP) isoforms which are key for brain function. SynGAP C‐termini splice variants show different spatio‐temporal expression and subcellular localization in the developing mouse brain. This study reveals a non‐synaptic and heterogenous role of SynGAP spliced variants. Depicted abundance differences only allow relative comparison within a given tissue (top panel), postnatal age (PND, middle panel), or subcellular distribution (bottom panel). Ctx, cortex; Hip, hippocampus; Str, striatum; OB, Olfactory Bulb; Crb, cerebellum and tSynGAP, total SynGAP.
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- 2019
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11. Author response: Metazoan evolution of glutamate receptors reveals unreported phylogenetic groups and divergent lineage-specific events
- Author
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Hector Escriva, Demian Burguera, Esther Gratacòs-Batlle, Jie Ji, Nerea Roher, Rita Reig-Viader, David Ramos-Vicente, Pablo Fuentes-Prior, Àlex Bayés, Gemma Gou, Jordi Garcia-Fernàndez, Enrique Navas-Perez, David Soto, and Javier Luís
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Lineage specific ,Phylogenetic tree ,Evolutionary biology ,Glutamate receptor ,Biology - Published
- 2018
12. Chronic treatment with a MEK inhibitor reverses enhanced excitatory field potentials in Syngap1
- Author
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Maksym V. Kopanitsa, Noboru H. Komiyama, Seth G. N. Grant, Nurudeen O. Afinowi, Àlex Bayés, and Gemma Gou
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Male ,Long-Term Potentiation ,Hippocampus ,Hyperphosphorylation ,SYNGAP1 ,Membrane Potentials ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Animals ,PD-0325901 ,Synaptic transmission ,Pharmacology ,Chemistry ,MEK inhibitor ,Diphenylamine ,Long-term potentiation ,General Medicine ,MEK ,Cell biology ,ERK ,030104 developmental biology ,ras GTPase-Activating Proteins ,Benzamides ,Mutation ,Excitatory postsynaptic potential ,Female ,Postsynaptic density ,030217 neurology & neurosurgery - Abstract
Background: Synaptic Ras-GTPase-activating protein 1 (SYNGAP1) is an abundant brain-specific protein localized at the postsynaptic density of mammalian excitatory synapses. SYNGAP1 functions as a crucial regulator of downstream intracellular signaling triggered by N-methyl-D-aspartate receptor activation. One of the most important signaling pathways regulated by SYNGAP1 is the Ras-Raf-MEK-ERK pathway. SYNGAP1 deficiency is associated with hyperphosphorylation of MEK and ERK kinases and with altered synaptic function in Syngap1(+/-) mice. Loss-of-function mutations in the SYNGAP1 gene have been documented in many human cognitive and neurological disorders. However, there are currently no approaches that reverse the phenotypes of SYNGAP1 deficiency. Methods: Using electrophysiological recordings of field responses in hippocampal slices, we examined if disturbances of synaptic physiology in the hippocampus of 7-8-month old Syngapr1(+/-) mice were sensitive to the effect of the MEK inhibitor PD-0325901 given orally for 6 days. Results: We found that in hippocampal slices from vehicle-treated Syngap1(+/-) mice, basal synaptic responses were higher and their long-term potentiation (LTP) was lower than in slices from wild-type littermates. Chronic administration of PD-0325901 normalized basal synaptic responses, but did not reverse LTP deficit. Conclusions: The differential sensitivity of basal synaptic transmission and LTP to MEK inhibition indicates that the effects of SYNGAP1 deficiency on these synaptic parameters are mediated by distinct pathways. Our findings also suggest that at least some physiological phenotypes of the germline Syngap1 mutation can be ameliorated by pharmacological treatment of adult animals. (C) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.
- Published
- 2017
13. Effects of treatment with a carbon monoxide-releasing molecule and a heme oxygenase 1 inducer in the antinociceptive effects of morphine in different models of acute and chronic pain in mice
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Arnau Hervera, Olga Pol, Sergi Leánez, and Gemma Gou
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Nitric Oxide Synthase Type II ,Protoporphyrins ,Nitric Oxide Synthase Type I ,Pharmacology ,Allodynia ,Nitric oxide ,Antinociception ,Mice ,chemistry.chemical_compound ,Organometallic Compounds ,medicine ,Animals ,Inducer ,Carbon monoxide ,Mice, Knockout ,Analgesics ,Carbon Monoxide ,Behavior, Animal ,Morphine ,Chemistry ,Chronic pain ,Visceral pain ,medicine.disease ,Acute Pain ,COPP ,Heme oxygenase ,Disease Models, Animal ,Hyperalgesia ,Drug Therapy, Combination ,Chronic Pain ,medicine.symptom ,Heme Oxygenase-1 ,medicine.drug - Abstract
Treatment with a carbon monoxide-releasing molecule (tricarbonyldichlororuthenium(II) dimer, CORM-2) or a classical heme oxygenase 1 inducer (cobalt protoporphyrin IX, CoPP) has potent anti-inflammatory effects, but the role played by these treatments in the antinociceptive effects of morphine during acute and chronic pain was not evaluated. In wild type (WT), neuronal (NOS1-KO), or inducible (NOS2-KO) nitric oxide synthases knockout mice, we evaluated the effects of CORM-2 and CoPP treatments in the antinociceptive actions of morphine and their interaction with nitric oxide during acute, visceral, and chronic inflammatory or neuropathic pain. Acute and visceral pain was assessed through formalin and acid acetic writhing tests. Chronic inflammatory pain induced by the intra-articular administration of complete Freund's adjuvant and neuropathic pain by partial ligation of sciatic nerve were evaluated by measuring allodynia and hyperalgesia using the von Frey filaments, plantar, or cold plate tests. While nitric oxide, synthetized by NOS1 and/or NOS2, increased the local antinociceptive effects of morphine during acute and chronic pain, it decreased the inhibitory effects of morphine after visceral pain. Moreover, while CORM-2 or CoPP treatments did not alter or reduced the antinociceptive effects of morphine during acute and visceral pain, both treatments improved the local antiallodynic and antihyperalgesic effects of morphine after chronic inflammatory or neuropathic pain in WT, but not in KO mice. CORM-2 and CoPP treatments improved the local antinociceptive effects of morphine during chronic inflammatory and neuropathic pain by interaction with nitric oxide synthetized by NOS1 and NOS2 isoforms.
- Published
- 2013
14. Evolution of complexity in the zebrafish synapse proteome
- Author
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Àlex, Bayés, Mark O, Collins, Rita, Reig-Viader, Gemma, Gou, David, Goulding, Abril, Izquierdo, Jyoti S, Choudhary, Richard D, Emes, and Seth G N, Grant
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Male ,Genome ,Proteome ,Brain ,Post-Synaptic Density ,Nerve Tissue Proteins ,Zebrafish Proteins ,Models, Biological ,Article ,Mice ,Microscopy, Electron, Transmission ,Species Specificity ,Gene Duplication ,Synapses ,Animals ,Female ,Zebrafish ,Synaptosomes - Abstract
The proteome of human brain synapses is highly complex and is mutated in over 130 diseases. This complexity arose from two whole-genome duplications early in the vertebrate lineage. Zebrafish are used in modelling human diseases; however, its synapse proteome is uncharacterized, and whether the teleost-specific genome duplication (TSGD) influenced complexity is unknown. We report the characterization of the proteomes and ultrastructure of central synapses in zebrafish and analyse the importance of the TSGD. While the TSGD increases overall synapse proteome complexity, the postsynaptic density (PSD) proteome of zebrafish has lower complexity than mammals. A highly conserved set of ∼1,000 proteins is shared across vertebrates. PSD ultrastructural features are also conserved. Lineage-specific proteome differences indicate that vertebrate species evolved distinct synapse types and functions. The data sets are a resource for a wide range of studies and have important implications for the use of zebrafish in modelling human synaptic diseases., Systematic analysis of the zebrafish synapse proteome has been lacking. Here the authors characterize the ultrastructure of zebrafish synapse and compare the proteomes of postsynaptic density in zebrafish and mice, offering a resource for future studies using zebrafish to model diseases.
- Published
- 2016
15. The role of gaseous neurotransmitters in the antinociceptive effects of morphine during acute thermal pain
- Author
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Sergi Leánez, Gemma Gou, and Olga Pol
- Subjects
Male ,Nociception ,Metalloporphyrins ,Nitric Oxide Synthase Type II ,Protoporphyrins ,Pain ,Nitric Oxide Synthase Type I ,Pharmacology ,Nitric oxide ,Antinociception ,Gene Knockout Techniques ,Mice ,chemistry.chemical_compound ,Organometallic Compounds ,medicine ,Animals ,Hot plate test ,Carbon monoxide ,Analgesics ,Carbon Monoxide ,Neurotransmitter Agents ,Thermal nociception ,biology ,Morphine ,Temperature ,Membrane Proteins ,Drug Synergism ,Acute Pain ,COPP ,Heme oxygenase ,Nitric oxide synthase ,chemistry ,biology.protein ,Licking ,Heme Oxygenase-1 ,medicine.drug - Abstract
Treatment with a carbon monoxide-releasing molecule (tricarbonyldichlororuthenium(II) dimer, CORM-2) or a classical inducible heme oxygenase (HO-1) inducer (cobalt protoporphyrin IX, CoPP) enhanced the antinociceptive effects of morphine during chronic pain but the role played by these compounds in acute thermal nociception was not evaluated. The effects of CORM-2 and CoPP treatments on the local antinociceptive actions of morphine and their interactions with nitric oxide during acute pain were evaluated by using wild type (WT), neuronal (nNOS-KO) or inducible (iNOS-KO) nitric oxide synthase knockout mice and assessing their thermal nociception to a hot stimulus with the hot plate test. Our results showed that the absence of nNOS or iNOS genes did not alter licking and jumping responses nor the antinociceptive effects produced by morphine indicating that the local thermal inhibitory effects produced by this drug in the absence of inflammation or injury are not mediated by the nitric oxide pathway triggered by nNOS or iNOS enzymes. Moreover, while the systemic administration of CORM-2 or CoPP inhibited licking and jumping latencies in all genotypes, these treatments only enhanced the local inhibition of jumping latencies produced by morphine in WT and nNOS-KO mice which effects were reversed by the peripheral administration of an HO-1 inhibitor. These data indicate that the co-administration of morphine with CORM-2 or CoPP produced remarkable local antinociceptive effects in WT and nNOS-KO mice and reveal that a significant interaction between carbon monoxide and nitric oxide systems occurs on the local antinociceptive effects produced by morphine during acute thermal nociception.
- Published
- 2014
16. Video Conferencing in the Intravitreal Injection Clinic in Response to the COVID-19 Pandemic
- Author
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Habiba Saedon, Gemma Gould, Minara Begum, and Tariq M. Aslam
- Subjects
COVID-19 ,Tele-ophthalmology ,Visual acuity ,Ophthalmology ,RE1-994 - Abstract
Abstract Purpose To share a useful intervention to minimize risk of COVID-19 infection to both healthcare workers and patients in the eye clinic. Methods We present our experience of virtual, within-clinic remote visual acuity assessment to reduce the risk of infection with COVID-19. Results Along with standard recommendations for personal protective equipment and hand hygiene to contain viral spread and treating only urgent cases, remote within-clinic visual acuity testing and consultations can be undertaken with minimal specialist equipment and appears to provide useful information whilst being acceptable to patients. Conclusion Ophthalmology practice must adapt in order to combat COVID-19. This measure can easily be incorporated into daily practice to reduce both patient footfall within the department and close contact between patient and healthcare practitioners.
- Published
- 2020
- Full Text
- View/download PDF
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