Specificity of function of acetylcholinergic receptors in the caudate and vestibular nuclei.

采用大鼠脑片制片法进行电生理研究，以探讨尾状核和前庭核中乙酰胆碱受体的调节机制。卡巴胆碱或米斯卡林均呈剂量依赖性地抑制由尾状核局部刺激引起的细胞外动作电位。乙酰胆碱和毒扁豆碱联合应用也可抑制顺行反应，但尼古丁对神经元活动无影响。卡巴胆碱或毒扁豆碱可降低兴奋性突触后电位的幅度，增加细胞内去极化脉冲对细胞的放电，而尼古丁不影响这些电位。阿托品可阻断氨基甲胆碱的抑制和兴奋作用。这些结果表明，位于神经元突触前和突触后的M受体分别介导了尾状核胆碱能抑制和兴奋。多巴胺D-2激动剂溴隐亭使尾状核神经元的膜电位去极化，并使去极化脉冲引起的自发放电频率和动作电位数目增加。这种兴奋作用可被D-2拮抗剂多潘立酮和氟哌啶醇拮抗，但不被D-1拮抗剂SCH 23390拮抗。前庭内侧核神经元自发发放棘波。卡巴胆碱可剂量依赖性地增加神经元的自发放电，阿托品的加入可减弱卡巴胆碱引起的神经元兴奋。在毒扁豆碱存在的情况下，乙酰胆碱也增加了放电频率，而尼古丁则没有影响。这些结果提示，前庭内侧核自发活动神经元的放电频率受乙酰胆碱通过M受体调节。

Electrophysiological studies, using slice preparation of the rat brain, were undertaken to examine the regulatory mechanism of acetylcholine receptors in the caudate and vestibular nuclei. Either carbachol or milscarine dosedependently inhibited extracellular action potentials orthodromically elicited by local stimulation in the caudate nucleus. A combination of acetylcholine with physostigmine also inhibited the orthodromic responses, but nicotine had no effects on the neuronal activity. Carbachol or muscarine decreased the amplitude of excitatory postsynaptic potential and increased firing induced by intracellular depolarizing pulsesinto the cells, whereas nicotine did not affect these potentials. The inhibitory and excitatory effects of carbachol were blocked by atropine. These results suggest that muscarinic receptors located on the presynaptic and postsynaptic sites of the neuron mediate cholinergic inhibition and excitation in the caudate nucleus, respectively.Bromocriptine, a dopamine D-2 agonist, produced a depolarization of the membrane potential of the caudate neurons, and an increase in the spontaneous firing rate as well as the number of action potentials evoked by depolarizing pulses applied into the cells. The bromocriptine-induced excitation was antagonized by domperidone (D-2 antagonist) and haloperidol, but not affected by SCH 23390 (D-1 antagonist). The medial vestibular nucleus neurons fired spikes spontaneously. Carbachol dose-dependently increased the spontaneous firing, and the addition of atropine attenuated the carbachol-induced excitation of the neurons. Acetylcholine in the presence of physostigmine also increased the firing rate, while nicotine had no effects. These results suggest that firing rate of the spontaneously active neurons in the medial vestibular nucleus are regulated by acetylcholine via muscarinic receptors.