Frazier C J, Rollins Y D, Hall M E, Young D A, Rose G M
Neuroscience Training Program, University of Colorado Health Sciences Center, Denver, USA.
Brain Res. 1996 Jul 15;727(1-2):217-20. doi: 10.1016/0006-8993(96)00402-7.
We tested whether cholinergic denervation of the hippocampus of young rats would result in an enhancement of CA1 pyramidal cell responsiveness to nicotine. Electrolytic lesions of the medial septal area were performed in young male Fisher 344 rats. One month later the rats were anesthetized with pentobarbital and nicotine was locally applied to CA1 pyramidal neurons using pressure microejection. The dose of nicotine required to excite the pyramidal neurons was significantly lower for cells recorded from rats with septal lesions. However, no changes in hippocampal cytisine or alpha-bungarotoxin binding were found.
我们测试了幼鼠海马体的胆碱能去神经支配是否会导致CA1锥体细胞对尼古丁的反应性增强。对年轻雄性Fisher 344大鼠进行内侧隔区的电解损伤。一个月后，用戊巴比妥麻醉大鼠，并使用压力微注射将尼古丁局部施加于CA1锥体细胞。对于从有隔区损伤的大鼠记录的细胞，激发锥体细胞所需的尼古丁剂量显著更低。然而，未发现海马体中野靛碱或α-银环蛇毒素结合的变化。
