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多巴胺的抑制作用涉及新纹状体神经元中一种阈下的对铯离子(Cs⁺)敏感的电导。

Inhibitory action of dopamine involves a subthreshold Cs(+)-sensitive conductance in neostriatal neurons.

作者信息

Pacheco-Cano M T, Bargas J, Hernández-López S, Tapia D, Galarraga E

机构信息

Departamento de Neurociencias, Instituto de Fisiología Celular, UNAM, Mexico City, DF, Mexico.

出版信息

Exp Brain Res. 1996 Jul;110(2):205-11. doi: 10.1007/BF00228552.

Abstract

Intracellular recordings in in vitro slice preparations of rat brain were used to compare the actions of dopamine and dopamine receptor agonists on the subthreshold membrane properties of neostriatal neurons. A reproducible response for dopaminergic agonists was evoked after firing produced by current ramp injections that induced a subthreshold voltage displacement. Dopamine (10-100 microM) decreased both firing rate and membrane slope input resistance in virtually all cells tested. Input resistance change appeared as an increase in inward rectification. Approximate reversal potential was around -87 mV. The D1 receptor agonists SKF 38393 and Cl-APB (1-10 microM) mimicked both dopamine effects with a reversal potential around -89 mV. The effects were blocked by the presence of 5-10 mM caesium (Cs+) but not by 1 microM tetrodotoxin, suggesting that main D1 effects on input resistance are due to subthreshold Cs(+)-sensitive conductances. cAMP analogues mimicked the actions of D1 receptor agonists. The D2 agonist, quinpirole (1-10 microM), did not produce any input resistance change, nonetheless, it still produced a decrease in firing rate. This suggests that the main D2 effect on firing is due to actions on suprathreshold ion conductances. All effects were blocked by D1 and D2 antagonists, respectively. D1 or D2 effects were found in the majority of cells tested.

摘要

利用大鼠脑体外切片制备中的细胞内记录,比较多巴胺和多巴胺受体激动剂对新纹状体神经元阈下膜特性的作用。在由电流斜坡注射产生的诱发阈下电压位移的放电后,可诱发对多巴胺能激动剂的可重复反应。多巴胺(10 - 100微摩尔)几乎使所有测试细胞的放电率和膜斜率输入电阻降低。输入电阻变化表现为内向整流增加。近似反转电位约为 - 87毫伏。D1受体激动剂SKF 38393和Cl - APB(1 - 10微摩尔)模拟了多巴胺的两种效应,反转电位约为 - 89毫伏。这些效应被5 - 10毫摩尔铯(Cs +)阻断,但不被1微摩尔河豚毒素阻断,这表明D1对输入电阻的主要作用是由于阈下Cs(+)敏感电导。环磷酸腺苷类似物模拟了D1受体激动剂的作用。D2激动剂喹吡罗(1 - 10微摩尔)没有引起任何输入电阻变化,尽管如此,它仍然使放电率降低。这表明D2对放电的主要作用是由于对阈上离子电导的作用。所有效应分别被D1和D2拮抗剂阻断。在大多数测试细胞中发现了D1或D2效应。

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