Robinson J K, Zocchi A, Pert A, Crawley J N
Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, MD 20892, USA.
Brain Res. 1996 Feb 12;709(1):81-7. doi: 10.1016/0006-8993(95)01307-5.
Galanin-like immunoreactive terminals hyperinnervate the basal forebrain cholinergic neurons in Alzheimer's disease. To investigate the hypothesis that galanin acts directly on basal forebrain cell bodies, in vivo microdialysis studies were conducted in awake rats which analyzed the actions of galanin on acetylcholine release. Microinjection of galanin into the cholinergic cell body region of the medial septum-diagonal band (MS-DBB) inhibited acetylcholine release in the ventral hippocampus. These results are consistent with an interpretation that galanin terminals synapsing on cholinergic cell bodies of the basal forebrain may serve to inhibit the release of acetylcholine in the terminal fields of the cholinergic neurons.
在阿尔茨海默病中,甘丙肽样免疫反应性终末对基底前脑胆碱能神经元的支配过度。为了研究甘丙肽直接作用于基底前脑细胞体的假说,对清醒大鼠进行了体内微透析研究,分析了甘丙肽对乙酰胆碱释放的作用。向内侧隔 - 斜角带(MS - DBB)的胆碱能细胞体区域微量注射甘丙肽可抑制腹侧海马中的乙酰胆碱释放。这些结果符合这样一种解释,即与基底前脑胆碱能细胞体形成突触的甘丙肽终末可能起到抑制胆碱能神经元终末区域乙酰胆碱释放的作用。