2009 Fiscal Year Final Research Report
Analysis of the functional contribution of inhibitoru neuron and disinhibition in nociceptive processing: using genetically modified mice
| Project/Area Number |
19791058
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Gunma University |
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Principal Investigator |
ASO Chizu Gunma University, 大学院・医学系研究科, 助教 (40436308)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIKAWA Kouichi 群馬大学, 大学院・医学系研究科, 准教授 (00334110)
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| Project Period (FY) |
2007 – 2009
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| Keywords | 疼痛治療学 |
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| Research Abstract |
This study tested whether partial reductions in GABAergic inhibitory tone by GAD65 gene knockout [GAD65(-/-)] would contribute to the regulation of pain threshold in mice. In the hot plate test, which reflects supraspinal sensory integration, a significant reduction in the latency was observed for GAD65(-/-) mice. In the hot plate test, which reflects supraspinal sensory integration, a significant reduction in the latency was observed for GAD65(-/-) mice.We also measured GABA(A) receptor-mediated inhibitory postsynaptic currents in GAD65(-/-) mice and wild-type (WT) mice. Although properties of the phasic component of inhibitory postsynaptic currents were similar in both genotypes, tonic inhibition was significantly reduced in GAD65(-/-) mice. These results support the hypothesis that GAD65-mediated GABA synthesis plays significant roles in nociceptive processing via supraspinal mechanisms.
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