| Project/Area Number |
22591704
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | University of Toyama |
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Principal Investigator |
HIROTA Koki 富山大学, 大学院医学薬学研究部(医学), 准教授 (30218854)
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| Co-Investigator(Renkei-kenkyūsha) |
SASAKI Rika 富山大学, 大学院医学薬学研究部(医学), 助教 (10345572)
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| Project Period (FY) |
2010-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 認知症 / アルツハイマー病 / 海馬 / シナプス電位 / GABA / 全身麻酔薬 / 全身麻酔 / セボフルラン / 疾患モデルマウス / 抑制性シナプス伝達 / 再取り込み / 認知症モデルマウス |
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| Research Abstract |
Clinical anesthesiologists have an increasing opportunity to anesthetize elderly patients with dementia. In order to investigate whether the senile dementia modifies the anesthetic actions in the central nervous systems, we have studied effects of general anesthetics on the hippocampal synaptic transmission in the senescence-accelerated mice (SAM-P8 and SAM-R1). The characteristic feature of SAM-P8 mouse shows Alzheimer-type deficits in learning and memory, whereas SAM-R1 mouse has no neurological impairment. Field population spikes of CA1 pyramidal neurons were elicited, following the activation of recurrent inhibition. The pre-pulses were applied as train stimuli to activate release and then deplete GABA. Volatile and intravenous anesthetics had greater actions on inhibitory synaptic transmission in SAM-P8 than in SAM-R1, due to the increase in GABA release from presynaptic terminals.
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