INT9987
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Our data suggest that GABA receptors, which are coupled to Cl- channels, are also expressed by astrocytes in an intact tissue. | |||||||||||||||
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This projection coexpresses GABA and enkephalin, posing a role for mu-opioid receptors in the ventral pallidum in mediating the reinstatement of cocaine seeking. | |||||||||||||||
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The data also suggest that GABA(B) subunit gene expression may serve as a preclinical marker of antidepressant efficacy and of drug- or stress-induced modifications in central nervous system activity. | |||||||||||||||
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GABA(B) receptor function and subunit expression in the rat spinal cord as indicators of stress and the antinociceptive response to antidepressants. | |||||||||||||||
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Amitriptyline prevents thermal hyperalgesia and modifications in rat spinal cord GABA(B) receptor expression and function in an animal model of neuropathic pain. | |||||||||||||||
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The results indicate that partial sciatic nerve ligation decreases thermal and mechanical pain withdrawal latencies, and increases baclofen-stimulated [35S]GTPgammaS binding and GABA(B) receptor subunit gene expression in the rat lumbar spinal cord, suggesting that neuropathic pain may be due, in part, to a deficiency in GABAergic transmission. | |||||||||||||||
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In this study, we have investigated the effects of gabapentin on recombinant GABA(B(1a)) and GABA(B(1b)) receptors coexpressed with GABA(B(2)) in five different functional recombinant assays, its ability to inhibit [(3)H]GABA binding in a GABA(B) receptor-selective binding assay using rat synaptic membranes, and its ability to inhibit transient lower esophageal sphincter relaxations in Labrador retriever dogs. | |||||||||||||||
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Hence, the present study was undertaken to assess the peripheral analgesic, antiallodynic and antihyperalgesic activities of the synthesized structural analogues of GABA. | |||||||||||||||
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Differential expression of GABA(B(1b)) receptor mRNA in the thalamus of normal and monoarthritic animals. | |||||||||||||||
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In this study, we evaluated whether the expression of GABA(B(1b)) receptor mRNA is regulated supraspinally, namely in the thalamus, as part of the response to chronically enhanced noxious input arising from experimental monoarthritis (MA). | |||||||||||||||
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No expression of GABA(B(1b)) mRNA was found in the Rt of control or MA animals. | |||||||||||||||
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The amount of GABA(B(1b)) mRNA was expressed as times fold of background values. | |||||||||||||||
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The distribution of GABA(B(1b)) mRNA was determined bilaterally in the ventrobasal complex (VB), posterior (Po), centromedial/centrolateral (CM/CL) and reticular (Rt) thalamic nuclei. | |||||||||||||||
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We conclude that NO may be directly acting on GABA nerve terminals and tonically inhibiting GABA release or synthesis under basal conditions. | |||||||||||||||
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Experiments were undertaken to examine whether once daily i.p. administration of either of two antidepressants used for the treatment of neuropathic pain, amitriptyline (10 mg/kg) and fluoxetine (5 mg/kg), to rats for 7 days modifies GABA(B) receptor function and subunit expression in the lumbar spinal cord. | |||||||||||||||
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Differential regulation of GABA B receptor subunit expression and function. | |||||||||||||||
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The results indicate a lack of concordance between expression of GABA(B1) and GABA(B2) subunits and GABA(B) receptor function, suggesting these subunit proteins may serve multiple functions in the cells. | |||||||||||||||
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In the present study, experiments were undertaken to examine the relationship between GABA(B) receptor function and subunit expression in the rat lumbar spinal cord following pharmacological and physiological manipulation of this receptor system. | |||||||||||||||
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Although formalin-induced hind paw inflammation increases the production of GABA(B1) and GABA(B2) protein in the spinal cord within 24 h, there is no change in receptor function, as measured by the baclofen-stimulated guanosine 5'-O-(3-[(35)S]thiotriphosphate) ([(35)S]GTPgammaS) binding assay. | |||||||||||||||
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The GABA-transaminase-inhibitors decreased the striatal levels of the opioid peptides met-enkephalin and dynorphin(1-8) and concomitantly decreased the concentrations of the mRNAs coding for proenkephalin and prodynorphin. | |||||||||||||||
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