Freund R K, Wehner J M
J Neurogenet. 1987 Apr;4(2-3):75-86.
We used the hippocampal slice to examine extracellular electrophysiological responses to nicotine and the difference in sensitivity to nicotine-induced electrophysiological effects between the DBA and C3H mouse strains. Nicotine enhanced CA1 population spikes (PS) evoked by Schaffer collateral stimulation in a concentration-dependent manner (100 microM to 3.2 mM). This enhancement was slow to appear, achieving a maximum after 15 min. The enhanced PS was accompanied by the development of epileptiform activity (multiple PS's) at nicotine concentrations greater than or equal to 400 microM. Slices from DBA mice were significantly more sensitive than those from the C3H strain to these electrophysiological effects of nicotine. Mecamylamine (400 microM) blocked both the nicotine-induced PS enhancement and secondary population spikes in both strains, suggesting the involvement of nicotinic cholinergic receptors.
我们使用海马切片来检测对尼古丁的细胞外电生理反应,以及DBA和C3H小鼠品系对尼古丁诱导的电生理效应的敏感性差异。尼古丁以浓度依赖性方式(100微摩尔至3.2毫摩尔)增强了由Schaffer侧支刺激诱发的CA1群体峰电位(PS)。这种增强出现缓慢,15分钟后达到最大值。在尼古丁浓度大于或等于400微摩尔时,增强的PS伴随着癫痫样活动(多个PS)的出现。来自DBA小鼠的切片对尼古丁的这些电生理效应比来自C3H品系的切片明显更敏感。美加明(400微摩尔)阻断了两个品系中尼古丁诱导的PS增强和继发性群体峰电位,表明烟碱型胆碱能受体参与其中。