Scroggs R S, Cardenas C G, Whittaker J A, Kitai S T
Department of Anatomy and Neurobiology, Health Science Center, University of Tennessee, Memphis, Tennessee 38163, USA.
J Neurophysiol. 2001 Dec;86(6):2966-72. doi: 10.1152/jn.2001.86.6.2966.
The effect of muscarine on Ca2+ dependent electrical activity was studied in dopamine (DA) neurons located in the substantia nigra pars compacta (SNc) in brain slices from young rats, using sharp electrodes. In most DA neurons tested, muscarine (50 microM) reduced the amplitude of spontaneous oscillatory potentials and evoked Ca2+-dependent potentials recorded in the presence of TTX. Muscarine also reduced the amplitude of the slow afterhyperpolarization (sAHP) following action potentials in most DA neurons. These data suggest that muscarine reduces Ca2+ entry in SNc DA neurons. The reduction of the amplitude of the sAHP by muscarine in DA neurons may facilitate bursting initiated by glutamatergic input by increasing the frequency at which DA neurons can fire. The reduction of the sAHP via activation of muscarinic receptors in vivo may provide a mechanism whereby cholinergic inputs to DA neurons from the tegmental peduncular pontine nucleus could modulate dopamine release at dopaminergic targets in the brain.
使用尖锐电极,研究了毒蕈碱对幼鼠脑片黑质致密部(SNc)中多巴胺(DA)能神经元钙依赖性电活动的影响。在大多数测试的DA能神经元中,毒蕈碱(50微摩尔)降低了自发振荡电位的幅度,并降低了在存在河豚毒素(TTX)的情况下记录到的诱发钙依赖性电位的幅度。毒蕈碱还降低了大多数DA能神经元动作电位后的慢后超极化(sAHP)幅度。这些数据表明,毒蕈碱减少了SNc中DA能神经元的钙内流。毒蕈碱降低DA能神经元中sAHP的幅度可能通过增加DA能神经元放电频率来促进由谷氨酸能输入引发的爆发。在体内通过激活毒蕈碱受体降低sAHP可能提供一种机制,借此来自被盖脚桥被盖核的DA能神经元的胆碱能输入可以调节大脑中多巴胺能靶点处的多巴胺释放。