Dopamine receptor-mediated mechanisms involved in the expression of learned activity of primate striatal neurons.-猫眼课题宝

多巴胺受体介导的机制涉及灵长类纹状体神经元学习活动的表达。

DOI：

发表时间：

1998

期刊：

Journal of Neurophysiology

影响因子：

2.5

通讯作者：

中科院分区：

医学3区

文献类型：

作者：

K. Watanabe;M. Kimura

为了了解基底神经节神经元在行为学习期间和之后表达获得性活动的机制，在记录执行行为任务的猴子中纹状体神经元的活动时应用选择性多巴胺（DA）受体拮抗剂。在实验 1 中，一只猴子被训练将咔嗒声与一滴奖励水联系起来。使用不锈钢注射插管（内径300微米）通过微压施用DA受体拮抗剂，用于记录神经元活动的特氟龙涂层钨丝穿过该注射插管。在应用 D1 或 D2 类 DA 受体拮抗剂期间（总体积 <1 微升，速率为 1 微升/5-10 分钟），通过钨丝电极记录紧张性活跃神经元 (TAN)（灵长类纹状体中的一类神经元）对声音的反应。使用 D2 类拮抗剂 (-)-舒必利（20 微克/微升，58 mM，pH 6.8）消除了所检查的 5 个 TAN 中的 4 个的反应。在另外五个 TAN 中，D2 类拮抗剂和 D1 类拮抗剂 SCH23390（10 微克/微升，31 mM，pH 5.7）或顺式氟哌噻吨（30 微克/微升，59 mM，pH 6.6）均未显着抑制反应。在实验2中，将四管或五管玻璃微电极插入纹状体中。中央管用于细胞外 TAN 活性记录。每种 DA 受体拮抗剂均通过周围的一个桶进行离子电渗疗法。使用 SCH23390 (10 mM，pH 4.5) 和 (-)-舒必利 (10 mM，pH 4.5)。在 40 个 TAN 中检查了 D1 类和 D2 类拮抗剂的离子电渗疗法的效果。在进行记录的 40 个 TAN 中，19 个 TAN 中的反应仅被 D2 类拮抗剂抑制，3 个 TAN 中的反应仅被 D1 类拮抗剂抑制，7 个 TAN 中的反应被 D1 类和 D2 类拮抗剂两者抑制。当通过压力（<1 微升）或离子电渗疗法（<30 nA）施加 0.9% NaCl 盐水作为对照时，背景放电速率和 TAN 的响应均未受到显着影响。 TAN 的背景放电率也不受微压注射或离子电渗疗法应用的 D1 或 D2 类拮抗剂的影响。结论是，黑质纹状体 DA 系统使 TAN 主要通过纹状体中的 D2 类受体介导机制和部分通过 D1 类受体介导机制来表达学习活动。

To understand the mechanisms by which basal ganglia neurons express acquired activities during and after behavioral learning, selective dopamine (DA) receptor antagonists were applied while recording the activity of striatal neurons in monkeys performing behavioral tasks. In experiment 1, a monkey was trained to associate a click sound with a drop of reward water. DA receptor antagonists were administered by micropressure using a stainless steel injection cannula (300 microm ID) through which a Teflon-coated tungsten wire for recording neuronal activity had been threaded. Responses to sound by tonically active neurons (TANs), a class of neurons in the primate striatum, were recorded through a tungsten wire electrode during the application of either D1- or D2-class DA receptor antagonists (total volume <1 microl, at a rate of 1 microl/5-10 min). Application of the D2-class antagonist, (-)-sulpiride (20 micrograms/microl, 58 mM, pH 6.8), abolished the responses of four of five TANs examined. In another five TANs, neither the D2-class antagonist nor the D1-class antagonists, SCH23390 (10 micrograms/microl, 31 mM, pH 5.7) or cis-flupenthixol (30 micrograms/microl, 59 mM, pH 6.6) significantly suppressed responses. In experiment 2, four- or five-barreled glass microelectrodes were inserted into the striatum. The central barrel was used for extracellular recording of activity of TANs. Each DA receptor antagonist was iontophoretically applied through one of the surrounding barrels. SCH23390 (10 mM, pH 4.5) and (-)-sulpiride (10 mM, pH 4.5) were used. The effects of iontophoresis of both D1- and D2-class antagonists were examined in 40 TANs. Of 40 TANs from which recordings were made, responses were suppressed exclusively by the D2-class antagonist in 19 TANs, exclusively by the D1-class antagonist in 3 TANs, and by both D1- and D2-class antagonists in 7 TANs. When 0.9% NaCl, saline, was applied by pressure (<1 microl) or by iontophoresis (<30 nA) as a control, neither the background discharge rates nor the responses of TANs were significantly influenced. Background discharge rate of TANs was also not affected by D1- or D2-class antagonists applied by either micropressure injection or iontophoresis. It was concluded that the nigrostriatal DA system enables TANs to express learned activity primarily through D2-class and partly through D1-class receptor-mediated mechanisms in the striatum.