The effects of phencyclidine and N-allylnormetazocine on midbrain dopamine neuronal activity.
The effects of phencyclidine and N-allylnormetazocine on midbrain dopamine neuronal activity.
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DOI：
10.1016/0014-2999(84)90404-7
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发表时间：
1984-09
影响因子：
5
通讯作者：
Arthur S. Freeman;Benjamin S. Bunney
中科院分区：
文献类型：
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作者：
Arthur S. Freeman;Benjamin S. Bunney
采用单细胞记录技术研究了静脉和微电泳给予苯环利定（PCP）和N-烯丙基去甲甲唑辛（SKF-10，047）对中脑多巴胺（DA）神经元活动的影响。静脉注射PCP对黑质多巴胺（A9）和腹侧被盖（A10）DA神经元产生双相效应，随着剂量的增加，兴奋后抑制低于基线放电率。氟哌啶醇预处理可拮抗PCP引起的高剂量放电衰减，但不能拮抗PCP的兴奋效应。静脉注射（+）-和（−）-SKF-10，047增加了大多数A9和A10 DA神经元的放电率。与静脉注射的结果相反，离子电渗PCP通常仅对神经元活动产生非常弱的抑制作用，而（+）-和（−）-SKF-10，047没有产生一致的作用。结果表明，这些药物间接影响DA神经元的活动，这可能是一个属性所共享的药物分类为sigma受体激动剂。
Single unit recording techniques were used to determine the effects of intravenously and microiontophoretically administered phencyclidine (PCP) and the enantiomers of N-allylnormetazocine (SKF-10,047) on the activity of midbrain dopamine (DA) neurons. Intravenous PCP produced a biphasic effect on substantia nigra zona compacta (A9) and ventral tegmental (A10) DA neurons which consisted of excitation followed by inhibition below baseline firing rates as the dose was increased. The high-dose attenuation of firing by PCP, but not the excitatory effects, was antagonized by haloperidol pretreatment. Intravenous (+)- and (−)-SKF-10,047 increased the firing rate of most A9 and A10 DA neurons. In contrast to the intravenous findings, iontophoretic PCP generally exerted only very weak inhibitory actions on neuronal activity, while (+)- and (−)-SKF-10,047 produced no consistent effects. The results suggest that these drugs indirectly influence the activity of DA neurons and that this may be a property shared by drugs classified as sigma receptor agonists.