Modification of general anesthetic actions in hippocampus of the Alzheimer-type dementia model mice

临床麻醉师有越来越多的机会麻醉老年痴呆症患者。为了探讨老年性痴呆是否改变了中枢神经系统的麻醉作用，我们研究了全麻药对衰老加速小鼠(SAM-P8和SAM-R1)海马区突触传递的影响。SAM-P8小鼠的特征表现为学习和记忆方面的阿尔茨海默型缺陷，而SAM-R1小鼠没有神经损害。重复抑制激活后，CA1区锥体神经元的场区群峰电位被激发。预脉冲作为训练刺激，激活释放，然后耗尽GABA。挥发性麻醉剂和静脉麻醉剂对SAM-P8突触传递的抑制作用大于SAM-R1，这是由于突触前终末GABA释放增加所致。

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.