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帕金森病大鼠苍白球多巴胺 D1 样受体活性的调制。

Modulation of the activity of globus pallidus by dopamine D1-like receptors in parkinsonian rats.

机构信息

Department of Physiology, Qingdao University, Qingdao 266071, China.

出版信息

Neuroscience. 2011 Oct 27;194:181-8. doi: 10.1016/j.neuroscience.2011.08.011. Epub 2011 Aug 6.

DOI:10.1016/j.neuroscience.2011.08.011
PMID:21846496
Abstract

Morphological studies have shown that the globus pallidus receives dopaminergic innervation from the collaterals of nigrostriatal fibers. Dopamine D1-like receptors are expressed at both pre- and postsynaptic membrane. In the present study, we investigate the in vivo electrophysiological and behavioral effects of pallidal dopamine D1-like receptors in parkinsonian rats. On the lesioned side of 6-hydroxydopamine (6-OHDA) parkinsonian rats, micropressure ejection of dopamine D1-like receptor agonist, SKF38393, increased (88.2 ± 18.6%) the firing rate in 10 out of the 32 pallidal neurons, but decreased (49.5 ± 6.1%) the firing rate in 14 out of the 32 neurons. Furthermore, on the unlesioned side of parkinsonian rats, SKF38393 increased (43.0 ± 6.3%) the firing rate in 9 out of the 30 pallidal neurons, but decreased (47.1 ± 4.8%) the firing rate in 13 out of the 30 neurons. In behaving rats, unilateral microinjection of SKF38393 led to contralateral deflection in the presence of systemic haloperidol administration. The selective dopamine D1-like receptor antagonist, SCH23390, blocked both SKF38393-induced electrophysiological and behavioral effects. Combining electrophysiological and behavioral findings, we concluded that activation of dopamine D1-like receptors modulates the activity of globus pallidus neurons in rats.

摘要

形态学研究表明苍白球接受来自黑质纹状体纤维侧支的多巴胺能神经支配。多巴胺 D1 样受体在突触前膜和突触后膜均有表达。在本研究中,我们研究了帕金森病大鼠苍白球多巴胺 D1 样受体的体内电生理和行为效应。在 6-羟多巴胺(6-OHDA)帕金森病大鼠的损伤侧,多巴胺 D1 样受体激动剂 SKF38393 的微压喷射增加了 32 个苍白球神经元中的 10 个(88.2±18.6%)的放电率,但降低了 14 个神经元中的 14 个(49.5±6.1%)的放电率。此外,在帕金森病大鼠的未损伤侧,SKF38393 增加了 30 个苍白球神经元中的 9 个(43.0±6.3%)的放电率,但降低了 13 个神经元中的 13 个(47.1±4.8%)的放电率。在行为大鼠中,单侧微注射 SKF38393 导致在系统给予氟哌啶醇时出现对侧偏转。选择性多巴胺 D1 样受体拮抗剂 SCH23390 阻断了 SKF38393 诱导的电生理和行为效应。结合电生理和行为学发现,我们得出结论,激活多巴胺 D1 样受体调节大鼠苍白球神经元的活动。

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