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Mechanisms for establishment of GABA signaling in adrenal medullary chromaffin cells
Journal of Neurochemistry ( IF 4.2 ) Pub Date : 2021-03-11 , DOI: 10.1111/jnc.15345
Keita Harada 1 , Hidetada Matsuoka 1 , Yumiko Toyohira 2 , Yuchio Yanagawa 3 , Masumi Inoue 1
Affiliation  

γ-Aminobutyric acid (GABA) is thought to play a paracrine role in adrenal medullary chromaffin (AMC) cells. Comparative physiological and immunocytochemical approaches were used to address the issue of how the paracrine function of GABA in AMC cells is established. GABAA receptor Cl- channel activities in AMC cells of rats and mice, where corticosterone is the major glucocorticoid, were much smaller than those in AMC cells of guinea-pigs and cattle, where cortisol is the major. The extent of enhancement of GABAA receptor α3 subunit expression in rat pheochromocytoma (PC12) cells by cortisol was larger than that by corticosterone in parallel with their glucocorticoid activities. Thus, the species difference in GABAA receptor expression may be ascribed to a difference in glucocorticoid activity between corticosterone and cortisol. GABAA receptor Cl- channel activity in mouse AMC cells was enhanced by allopregnanolone, as noted with that in guinea-pig AMC cells, and the enzymes involved in allopregnanolone production were immunohistochemically detected in the zona fasciculata in both mice and guinea pigs. The expression of glutamic acid decarboxylase 67 (GAD67), one of the GABA synthesizing enzymes, increased after birth, whereas GABAA receptors already developed at birth. Stimulation of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors, but not nicotinic or muscarinic receptors, in PC12 cells, resulted in an increase in GAD67 expression in a protein-kinase A-dependent manner. The results indicate that glucocorticoid and PACAP are mainly responsible for the expressions of GABAA receptors and GAD67 involved in GABA signaling in AMC cells, respectively.

中文翻译:

GABA信号在肾上腺髓质嗜铬细胞中的建立机制

γ-氨基丁酸 (GABA) 被认为在肾上腺髓质嗜铬 (AMC) 细胞中起旁分泌作用。比较生理学和免疫细胞化学方法用于解决 GABA 在 AMC 细胞中的旁分泌功能如何建立的问题。以皮质酮为主要糖皮质激素的大鼠和小鼠AMC细胞中GABA A受体Cl -通道活性远小于以皮质醇为主的豚鼠和牛AMC细胞中的GABA A受体Cl -通道活性。皮质醇对大鼠嗜铬细胞瘤 (PC12) 细胞GABA A受体α3 亚基表达的增强程度大于皮质酮与其糖皮质激素活性的增强程度。因此,GABA A的物种差异受体表达可能归因于皮质酮和皮质醇之间糖皮质激素活性的差异。小鼠 AMC 细胞中GABA A受体 Cl -通道活性被别孕酮增强,正如在豚鼠 AMC 细胞中所注意到的那样,并且在小鼠和豚鼠的束状带中免疫组织化学检测到参与别孕酮生产的酶。GABA 合成酶之一的谷氨酸脱羧酶 67 (GAD67) 的表达在出生后增加,而 GABA A受体在出生时就已经发育。在 PC12 细胞中刺激垂体腺苷酸环化酶激活多肽 (PACAP) 受体,而不是烟碱或毒蕈碱受体,导致 GAD67 表达以蛋白激酶 A 依赖性方式增加。结果表明,糖皮质激素和PACAP分别主要负责AMC细胞中参与GABA信号传导的GABA A受体和GAD67的表达。
更新日期:2021-03-11
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