Feng Chun-Sheng, Wang Yun, Ma Hai-Chun, Yue Yun
Department of Anesthesiology, First Hospital of Jilin University, Changchun 130021, China.
Zhonghua Yi Xue Za Zhi. 2009 Aug 18;89(31):2206-9.
To determine effect of central neuronal nicotinic receptor on synaptic long-term potentiation (LTP) in the CA1 area of rats hippocampal slices.
Brain slice preparation transverse hippocampal slices were obtained from male Sprague-Dawley rats that were ether-anesthetized and decapitated. The hippocampus was rapidly removed, and slices were prepared in ice-cold artificial cerebrospinal fluid (ACSF), oxygenated with 95% O2 - 5% CO2. Seventy-seven slices were randomly divided into 11 equal groups (n = 7 each): group LTP; group isoflurane 0.125; group isoflurane 0.25; group isoflurane 0.5; group nicotine 0.1; group nicotine 1.0; group nicotine 10.0; group nicotine 1.0 + isoflurane 0.25; group nicotine 10.0 + isoflurane 0.25; group mecamylamine; group mecamylamine + isoflurane 0.125. One recording electrode was positioned in the pyramidal cell layer of the CA1 area of rats hippocampal slices to simultaneously record evoked population spikes (PS). For LTP induction, high-frequency stimulation (HFS) conditioning pulses (100 Hz/s) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode. The changes of PS amplitude after HFS were analyzed in each group.
The PS amplitude of the rats hippocampal slices in group LTP after HFS was significantly increased by (52 +/- 12)% compared with that of pre-HFS indicating the successful induction of LTP. Compared with group LTP, the PS amplitudes decreased significantly in group isoflurane 0.125, 0.25 and 0.5 after HFS (P < 0.01) and increased significantly in group nicotine 1.0 and 10.0 (P < 0.01), but the PS amplitudes in group nicotine 0.1 was not significantly changed after HFS (P > 0.05). The PS amplitudes after HFS in group nicotine 1.0 + isoflurane 0.25 and group nicotine 10.0 + isoflurane 0.25 was dramatically increased compared with the value of group isoflurane 0.25 (P < 0.01), but did not differ significantly from group LTP (P > 0.05). The PS amplitudes after HFS in group mecamylamine has no significant difference compared with the value of group isoflurane 0.125, but it was significantly lower than that in group LTP (P < 0.01). The PS amplitudes after HFS in group mecamylamine + isoflurane 0.125 significantly decreased compared with the value of group isoflurane 0.125 and group LTP (P < 0.05 or P < 0.01).
The inhibition of LTP induction may contribute to isoflurane-induced deficits in memory, and the underlying mechanism is involved in the inhibition of nicotinic acetylcholine receptor activation in hippocampus of rats.
确定中枢神经元烟碱样受体对大鼠海马脑片CA1区突触长时程增强（LTP）的影响。
脑片制备 将雄性Sprague-Dawley大鼠用乙醚麻醉后断头，迅速取出海马，在冰冷的人工脑脊液（ACSF）中制备脑片，用95% O₂ - 5% CO₂ 进行氧合。77片脑片随机分为11个相等的组（每组n = 7）：LTP组；异氟烷0.125组；异氟烷0.25组；异氟烷0.5组；尼古丁0.1组；尼古丁1.0组；尼古丁10.0组；尼古丁1.0 + 异氟烷0.25组；尼古丁10.0 + 异氟烷0.25组；美加明组；美加明 + 异氟烷0.125组。将一个记录电极置于大鼠海马脑片CA1区的锥体细胞层，同时记录诱发群体峰电位（PS）。为诱导LTP，使用双极刺激电极对海马的Schaffer侧支-连合通路施加高频刺激（HFS）条件脉冲（100 Hz/s）。分析每组HFS后PS幅度的变化。
LTP组大鼠海马脑片HFS后PS幅度比HFS前显著增加（52±12）%，表明成功诱导了LTP。与LTP组相比，异氟烷0.125、0.25和0.5组HFS后PS幅度显著降低（P < 0.01），尼古丁1.0和10.0组显著增加（P < 0.01），但尼古丁0.1组HFS后PS幅度无显著变化（P > 0.05）。尼古丁1.0 + 异氟烷0.25组和尼古丁10.0 + 异氟烷0.25组HFS后的PS幅度与异氟烷0.25组相比显著增加（P < 0.01），但与LTP组无显著差异（P > 0.05）。美加明组HFS后的PS幅度与异氟烷0.125组相比无显著差异，但显著低于LTP组（P < 0.01）。美加明 + 异氟烷0.125组HFS后的PS幅度与异氟烷0.125组和LTP组相比显著降低（P < 0.05或P < 0.01）。
LTP诱导的抑制可能导致异氟烷引起的记忆缺陷，其潜在机制涉及对大鼠海马中烟碱样乙酰胆碱受体激活的抑制。
