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纹状体输入及毒蕈碱受体对苍白球放电的速率依赖性效应。

Striatal input- and rate-dependent effects of muscarinic receptors on pallidal firing.

作者信息

Querejeta Enrique, Alatorre Alberto, Ríos Alain, Barrientos Rafael, Oviedo-Chávez Aldo, Bobadilla-Lugo Rosa Amalia, Delgado Alfonso

机构信息

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, 11340 México, DF, Mexico.

出版信息

ScientificWorldJournal. 2012;2012:547638. doi: 10.1100/2012/547638. Epub 2012 May 1.

DOI:10.1100/2012/547638
PMID:22654627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3361291/
Abstract

The globus pallidus (GP) plays a key role in the overall basal ganglia (BG) activity. Despite evidence of cholinergic inputs to GP, their role in the spiking activity of GP neurons has not received attention. We examine the effect of local activation and blockade of muscarinic receptors (MRs) in the spontaneous firing of GP neurons both in normal and ipsilateral striatum-lesioned rats. We found that activation of MRs produces heterogeneous responses in both normal and ipsilateral striatum-lesioned rats: in normal rats the response evoked by MRs depends on the predrug basal firing rate; the inhibition evoked by MRs is higher in normal rats than in striatum-lesioned rats; the number of neurons that undergo inhibition is lower in striatum-lesioned rats than in normal rats. Our data suggest that modulation of MRs in the GP depends on the firing rate before their activation and on the integrity of the striato-pallidal pathway.

摘要

苍白球（GP）在整个基底神经节（BG）活动中起关键作用。尽管有证据表明胆碱能传入纤维进入GP，但其在GP神经元放电活动中的作用尚未受到关注。我们研究了在正常大鼠和同侧纹状体损伤大鼠中，局部激活和阻断毒蕈碱受体（MRs）对GP神经元自发放电的影响。我们发现，MRs的激活在正常大鼠和同侧纹状体损伤大鼠中均产生异质性反应：在正常大鼠中，MRs诱发的反应取决于给药前的基础放电率；MRs诱发的抑制作用在正常大鼠中高于纹状体损伤大鼠；纹状体损伤大鼠中受到抑制的神经元数量低于正常大鼠。我们的数据表明，GP中MRs的调节取决于其激活前的放电率以及纹状体-苍白球通路的完整性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/c6bb47ae4731/TSWJ2012-547638.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/2215a2d4d4f3/TSWJ2012-547638.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/e3b094502ff9/TSWJ2012-547638.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/09068c92f096/TSWJ2012-547638.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/9d884a97fd44/TSWJ2012-547638.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/c6bb47ae4731/TSWJ2012-547638.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/2215a2d4d4f3/TSWJ2012-547638.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/e3b094502ff9/TSWJ2012-547638.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/09068c92f096/TSWJ2012-547638.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/9d884a97fd44/TSWJ2012-547638.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03b1/3361291/c6bb47ae4731/TSWJ2012-547638.005.jpg

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