Effects of phencyclidine on ventral tegmental A10 dopamine neurons in the rat.

Effects of phencyclidine on ventral tegmental A10 dopamine neurons in the rat.
复制标题

苯环己哌啶对大鼠腹侧被盖 A10 多巴胺神经元的影响。

DOI:
10.1016/0028-3908(86)90246-7
复制
发表时间:
1986
期刊:
影响因子:
4.7
通讯作者:
French,ED
French,ED
中科院分区:
医学2区
文献类型:
--
作者:
French,ED

文献摘要

相似文献

细胞外单单位记录被用来确定全身应用和离子导入苯环利定对大鼠腹侧被盖区内电生理识别的A10多巴胺神经元的影响。静脉注射苯环利定对A10细胞既有抑制作用,也有兴奋作用。注射氟哌啶醇可完全逆转苯环利定引起的抑制作用的约42%。苯环利定的兴奋作用最常导致去极化失活状态,对氟哌啶醇不敏感。在利血平和α-甲基-对酪氨酸联合处理的所有动物中,全身应用苯环利定可有效地防止A100细胞活性的改变,这会耗尽中枢儿茶酚胺储备的90%以上。与静脉注射获得的数据相反,离子导入应用苯环利定仅对A10细胞的活动产生抑制,在少数情况下,放电频率的降低伴随着动作电位幅度的增加。多巴胺能神经元对全身应用和离子导入苯环利定的反应模式的比较表明,苯环利定诱导的兴奋不是在A10细胞体水平上介导的,而是通过腹侧被盖区以外的部位。这项研究的结果还表明,苯环利定对A10神经元活动的一些影响明显依赖于与多巴胺的相互作用,因此,将支持苯环利定可以作为间接多巴胺激动剂的假设。然而,与多巴胺没有明显联系的苯环利定的其他作用可能代表了药理上不同的A100神经元亚群对苯环利定的反应。
Extracellular single unit recordings were used to determine the effects of systemically and iontophoretically applied phencyclidine on electrophysiologically-identified A10dopamine neurons within the ventral tegmental area of the rat. Intravenous injections of phencyclidine inhibited, as well as excited A10cells. Approximately 42% of the inhibitions induced by phencyclidine were completely reversed by an injection of haloperidol. The excitatory effects of phencyclidine most often resulted in a state of depolarized inactivation and were not sensitive to haloperidol. The alteration of the activity of A10cells by systemically-applied phencyclidine was effectively prevented in all animals pretreated with a combination of reserpine and α-methyl-p-tyrosine, which depleted stores of central catecholamines by over 90%. In contrast to the data obtained with intravenous injections, iontophoretic applications of phencyclidine produced only inhibition of the activity of the A10cells and, in a few of these cases the decreased firing rate was accompanied by an increase in the amplitude of the action potential. A comparison of the response patterns of dopaminergic neurons to systemically- and iontophoretically-applied phencyclidine would suggest that excitations induced by phencyclidine are not mediated at the level of the A10cell bodies but through a site outside the ventral tegmental area. The results of this study also indicate that some of the effects of phencyclidine on the activity of A10neurons are clearly dependent upon an interaction with dopamine and thus, would support the hypothesis that phencyclidine can act as an indirect dopamine agonist. However, other effects of phencyclidine which are not apparently linked to dopamine may represent the response of a pharmacologically-distinct subpopulation of A10neurons to phencyclidine.