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CRF-R1 和 CB1 受体对面部刺激诱导的小鼠小脑皮层 MLI-PC 可塑性的相反作用。

Opposing actions of CRF-R1 and CB1 receptor on facial stimulation-induced MLI-PC plasticity in mouse cerebellar cortex.

机构信息

Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, 133002, Jilin, China.

Department of Osteology, Affiliated Hospital of Yanbian University, Yanji, 133000, Jilin, China.

出版信息

BMC Neurosci. 2022 Jun 26;23(1):39. doi: 10.1186/s12868-022-00726-8.

DOI:10.1186/s12868-022-00726-8
PMID:35754033
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9235104/
Abstract

BACKGROUND

Corticotropin-releasing factor (CRF) is the major neuromodulator orchestrating the stress response, and is secreted by neurons in various regions of the brain. Cerebellar CRF is released by afferents from inferior olivary neurons and other brainstem nuclei in response to stressful challenges, and contributes to modulation of synaptic plasticity and motor learning behavior via its receptors. We recently found that CRF modulates facial stimulation-evoked molecular layer interneuron-Purkinje cell (MLI-PC) synaptic transmission via CRF type 1 receptor (CRF-R1) in vivo in mice, suggesting that CRF modulates sensory stimulation-evoked MLI-PC synaptic plasticity. However, the mechanism of how CRF modulates MLI-PC synaptic plasticity is unclear. We investigated the effect of CRF on facial stimulation-evoked MLI-PC long-term depression (LTD) in urethane-anesthetized mice by cell-attached recording technique and pharmacological methods.

RESULTS

Facial stimulation at 1 Hz induced LTD of MLI-PC synaptic transmission under control conditions, but not in the presence of CRF (100 nM). The CRF-abolished MLI-PC LTD was restored by application of a selective CRF-R1 antagonist, BMS-763,534 (200 nM), but it was not restored by application of a selective CRF-R2 antagonist, antisauvagine-30 (200 nM). Blocking cannabinoid type 1 (CB1) receptor abolished the facial stimulation-induced MLI-PC LTD, and revealed a CRF-triggered MLI-PC long-term potentiation (LTP) via CRF-R1. Notably, either inhibition of protein kinase C (PKC) with chelerythrine (5 µM) or depletion of intracellular Ca with cyclopiazonic acid (100 µM), completely prevented CRF-triggered MLI-PC LTP in mouse cerebellar cortex in vivo.

CONCLUSIONS

The present results indicated that CRF blocked sensory stimulation-induced opioid-dependent MLI-PC LTD by triggering MLI-PC LTP through CRF-R1/PKC and intracellular Ca signaling pathway in mouse cerebellar cortex. These results suggest that activation of CRF-R1 opposes opioid-mediated cerebellar MLI-PC plasticity in vivo in mice.

摘要

背景

促肾上腺皮质释放因子 (CRF) 是协调应激反应的主要神经调节剂，由大脑各个区域的神经元分泌。在受到应激挑战时，来自下橄榄核神经元和其他脑干核的传入纤维会释放小脑 CRF，通过其受体参与调节突触可塑性和运动学习行为。我们最近发现，CRF 通过体内的 CRF 型 1 受体 (CRF-R1) 调节面部刺激诱发的分子层中间神经元-浦肯野细胞 (MLI-PC) 突触传递，表明 CRF 调节感觉刺激诱发的 MLI-PC 突触可塑性。然而，CRF 调节 MLI-PC 突触可塑性的机制尚不清楚。我们通过细胞贴附记录技术和药理学方法，研究了 CRF 对在体麻醉小鼠面部刺激诱发的 MLI-PC 长时程抑制 (LTD) 的影响。

结果

在对照条件下，1 Hz 的面部刺激诱导 MLI-PC 突触传递 LTD，但在 CRF（100 nM）存在下则不会。选择性 CRF-R1 拮抗剂 BMS-763534（200 nM）可恢复被 CRF 消除的 MLI-PC LTD，但选择性 CRF-R2 拮抗剂 antisauvagine-30（200 nM）则不能。阻断大麻素 1 型受体 (CB1) 则消除了面部刺激诱导的 MLI-PC LTD，并通过 CRF-R1 揭示了 CRF 触发的 MLI-PC 长时程增强 (LTP)。值得注意的是，使用 chelerythrine（5 µM）抑制蛋白激酶 C (PKC) 或用环匹阿尼酸 (100 µM) 耗尽细胞内 Ca2+，完全阻止了在体小鼠小脑皮层中 CRF 触发的 MLI-PC LTP。

结论

本研究结果表明，CRF 通过 CRF-R1/PKC 和细胞内 Ca2+信号通路触发 MLI-PC LTP，从而阻断感觉刺激诱导的、依赖阿片类物质的 MLI-PC LTD，这表明在体激活 CRF-R1 可拮抗小脑 MLI-PC 可塑性在小鼠体内的阿片样作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/052b6d7313ab/12868_2022_726_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/ffa993e6cd77/12868_2022_726_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/30827dcffbe2/12868_2022_726_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/3c3975c171eb/12868_2022_726_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/2b1ba1597cfd/12868_2022_726_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/29b0df74caa6/12868_2022_726_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/c55acf024e12/12868_2022_726_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/052b6d7313ab/12868_2022_726_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/ffa993e6cd77/12868_2022_726_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/30827dcffbe2/12868_2022_726_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/3c3975c171eb/12868_2022_726_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/2b1ba1597cfd/12868_2022_726_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/29b0df74caa6/12868_2022_726_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/c55acf024e12/12868_2022_726_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ffb/9235104/052b6d7313ab/12868_2022_726_Fig7_HTML.jpg

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