Shinba T, Sugita R, Watabe K
Brain Res Bull. 1985 Dec;15(6):579-86. doi: 10.1016/0361-9230(85)90207-2.
Three groups of meso-accumbens (Acc) neurons in the ventral tegmental area were differentiated by their antidromic discharge property; dopaminergic type 1 (n = 10), non-dopaminergic type 2 (n = 2) and unclassified (n = 2) neurons. During repetitive activation at 10 Hz, the latency of the initial segment (IS) spike, which was often not followed by the somadendritic (SD) spike, was gradually prolonged in type 1, but not in type 2 and unclassified neurons. The latency prolongation of type 1 neurons was reduced to about a half of the normal in rats treated with kainic acid plus haloperidol, but only slightly when treated with kainic acid or picrotoxin. The rate of SD invasion tended to increase after all kinds of chemical treatment. Stimulation of the medial forebrain bundle in type 1 neurons gave responses comparable to Acc stimulation. It is suggested that the latency prolongation of IS spike is produced mainly by axonal mechanism. But additional somatic mechanisms such as dopaminergic self-inhibition and GABAergic and non-GABAergic inputs from the Acc would make some contribution, and at the same time produce frequent suppression of the antidromic SD spike.
腹侧被盖区中脑伏隔核(Acc)的三组神经元通过其逆向放电特性得以区分:多巴胺能1型(n = 10)、非多巴胺能2型(n = 2)和未分类(n = 2)神经元。在10 Hz的重复激活过程中,起始节段(IS)峰电位的潜伏期(通常不伴随胞体树突(SD)峰电位)在1型神经元中逐渐延长,但在2型和未分类神经元中则不然。在用 kainic 酸加氟哌啶醇处理的大鼠中,1型神经元的潜伏期延长减少至正常的约一半,但在用 kainic 酸或印防己毒素处理时仅略有减少。在所有化学处理后,SD 侵入率均有增加的趋势。刺激1型神经元的内侧前脑束所产生的反应与刺激伏隔核相当。提示IS峰电位潜伏期延长主要由轴突机制产生。但额外的胞体机制,如多巴胺能自身抑制以及来自伏隔核的GABA能和非GABA能输入也会起一定作用,同时会频繁抑制逆向SD峰电位。