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糖皮质激素受体的激活可在体外迅速引发钙依赖性血清素释放。

Activation of the glucocorticoid receptor rapidly triggers calcium-dependent serotonin release in vitro.

机构信息

Department of Psychiatry and Psychotherapy, Biochemical Laboratory, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Transgenic Models, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

出版信息

CNS Neurosci Ther. 2021 Jul;27(7):753-764. doi: 10.1111/cns.13634. Epub 2021 Mar 14.

DOI:10.1111/cns.13634
PMID:33715314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8193689/
Abstract

AIMS

Glucocorticoids rapidly provoke serotonin (5-HT) release in vivo. We aimed to investigate molecular mechanisms of glucocorticoid receptor (GR)-triggered 5-HT release.

METHODS

Employing 1C11 cells to model 5-HT neurotransmission, immunofluorescence and Pearson's Correlation Coefficient were used to analyze colocalization of GR, 5-HT, vesicle membrane protein synaptotagmin 1 and vesicle dye FM4-64FX. FFN511 and FM4-64FX dyes as well as calcium imaging were used to visualize vesicular 5-HT release upon application of GR agonist dexamethasone, GR antagonist mifepristone and voltage-gated calcium channel (VGCC) inhibitors.

RESULTS

GR, 5-HT, synaptotagmin 1 and FM4-64FX showed overlapping staining patterns, with Pearson's Correlation Coefficient indicating colocalization. Similarly to potassium chloride, dexamethasone caused a release of FFN511 and uptake of FM4-64FX, indicating vesicular 5-HT release. Mifepristone, calcium depletion and inhibition of L-type VGCC significantly diminished dexamethasone-induced vesicular 5-HT release.

CONCLUSIONS

In close proximity to 5-HT releasing sites, activated GR rapidly triggers L-type VGCC-dependent vesicular 5-HT release. These findings provide a better understanding of the interrelationship between glucocorticoids and 5-HT release.

摘要

目的

糖皮质激素在体内能迅速引发血清素（5-HT）释放。本研究旨在探讨糖皮质激素受体（GR）触发 5-HT 释放的分子机制。

方法

采用 1C11 细胞模拟 5-HT 神经传递，通过免疫荧光和 Pearson 相关系数分析 GR、5-HT、囊泡膜蛋白突触结合蛋白 1 和囊泡染料 FM4-64FX 的共定位。应用 GR 激动剂地塞米松、GR 拮抗剂米非司酮和电压门控钙通道（VGCC）抑制剂，FFN511 和 FM4-64FX 染料及钙成像来可视化 GR 激动后囊泡 5-HT 的释放。

结果

GR、5-HT、突触结合蛋白 1 和 FM4-64FX 的染色模式存在重叠，Pearson 相关系数表明存在共定位。与氯化钾类似，地塞米松引起 FFN511 的释放和 FM4-64FX 的摄取，表明囊泡 5-HT 的释放。米非司酮、钙耗竭和 L 型 VGCC 抑制显著减少了地塞米松诱导的囊泡 5-HT 释放。

结论

在靠近 5-HT 释放部位的地方，激活的 GR 能迅速引发 L 型 VGCC 依赖性囊泡 5-HT 释放。这些发现有助于更好地理解糖皮质激素和 5-HT 释放之间的相互关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/5aa7ee6019d3/CNS-27-753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/c3ef80fe6aa4/CNS-27-753-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/9d21f8866562/CNS-27-753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/5ff88da023b1/CNS-27-753-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/371dc87bd293/CNS-27-753-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/5aa7ee6019d3/CNS-27-753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/c3ef80fe6aa4/CNS-27-753-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/9d21f8866562/CNS-27-753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/5ff88da023b1/CNS-27-753-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/371dc87bd293/CNS-27-753-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ecb/8193689/5aa7ee6019d3/CNS-27-753-g001.jpg

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