槟榔碱增强尼古丁在大鼠海马脑片CA1锥体细胞诱发PS2的作用

在大鼠离体海马脑片上，记录CA1锥体细胞外诱发群峰电位(PS)，以灌流和局部微量注射两种给药途径，观察了槟榔碱(Are)与尼古丁(Nic)同时给药对PS的影响，研究胆碱能M和N受体之间的关系. 结果表明，Are增强Nic诱发第二个群峰电位(PS2)的作用，这一作用不能被M受体拮抗剂阿托品(0.001-0.1 mmol·L^-1)或N受体拮抗剂美卡拉明(1.0 mmol·L^-1)拮抗，兼具中枢胆碱M和N受体拮抗作用的贝那替秦(0.01-0.1 mmol·L^-1)能较好地预防这一作用，表明M和N受体之间存在有相互调节关系.

Facilitatory effect of arecoline on nicotine induced second population spikes(PS2) of CA1 pyramidal cells in rat hippocampal slices

To estimate the relationship between muscarinic receptors(mAChR) and nicotinic receptors(nAChR), the influences of arecoline and nicotine applied simutaneously by bath and pressure ejection from micropipette on extracellular population spikes (PS) were studied. The PS evoked by stimulation of Schaffer collaterals were recorded from CA1 cell layer of hippocampal slices which were isolated from Wistar rats. The results showed that arecoline enhanced the incidence of nicotine-induced second PS(PS2). This facilitatory effect could not be blocked by atropine(0.001-0.1 mmol·L^-1) or mecamylamine(1.0 mmol·L^-1), but by benactyzine(0.01-0.1 mmol·L^-1), an antagonist with both antimuscarinic and antinicotinic activities. These results indicate that there might be interaction between mAChR and nAChR in the hippocampus.