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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Functional characterization of alpha9-containing cholinergic nicotinic receptors in the rat adrenal medulla: implication in stress-induced functional plasticity.
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Functional characterization of alpha9-containing cholinergic nicotinic receptors in the rat adrenal medulla: implication in stress-induced functional plasticity.

机译：大鼠肾上腺髓质中含α9的胆碱能烟碱样受体的功能表征：应激诱导的功能可塑性的含义。

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An increase in circulating adrenal catecholamine levels constitutes one of the mechanisms whereby organisms cope with stress. Accordingly, stimulus-secretion coupling within the stressed adrenal medullary tissue undergoes persistent remodeling. In particular, cholinergic synaptic neurotransmission between splanchnic nerve terminals and chromaffin cells is upregulated in stressed rats. Since synaptic transmission is mainly supported by activation of postsynaptic neuronal acetylcholine nicotinic receptors (nAChRs), we focused our study on the role of alpha9-containing nAChRs, which have been recently described in chromaffin cells. Taking advantage of their specific blockade by the alpha-conotoxin RgIA (alpha-RgIA), we unveil novel functional roles for these receptors in the stimulus-secretion coupling of the medulla. First, we show that in rat acute adrenal slices, alpha9-containing nAChRs codistribute with synaptophysin and significantly contribute to EPSCs. Second, we show that these receptors are involved in the tonic inhibitory control exerted by cholinergic activity on gap junctional coupling between chromaffin cells, as evidenced by an increased Lucifer yellow diffusion within the medulla in alpha-RgIA-treated slices. Third, we unexpectedly found that alpha9-containing nAChRs dominantly (>70%) contribute to acetylcholine-induced current in cold-stressed rats, whereas alpha3 nAChRs are the main contributing channels in unstressed animals. Consistently, expression levels of alpha9 nAChR transcript and protein are overexpressed in cold-stressed rats. As a functional relevance, we propose that upregulation of alpha9-containing nAChR channels and ensuing dominant contribution in cholinergic signaling may be one of the mechanisms whereby adrenal medullary tissue appropriately adapts to increased splanchnic nerve electrical discharges occurring in stressful situations.
机译：循环中的肾上腺儿茶酚胺水平升高是机体应对压力的机制之一。因此，在应激的肾上腺髓质组织内的刺激-分泌偶联经历了持续的重塑。特别地，在内脏神经末梢与嗜铬细胞之间的胆碱能突触神经传递在应激大鼠中被上调。由于突触传递主要受突触后神经元乙酰胆碱烟碱受体（nAChRs）的激活支持，因此我们将研究重点放在了含α9的nAChRs中，最近在嗜铬细胞中已有描述。利用α-芋螺毒素RgIA（alpha-RgIA）的特异性阻断作用，我们揭示了这些受体在延髓的刺激-分泌偶联中的新型功能作用。首先，我们显示在大鼠急性肾上腺切片中，含alpha9的nAChR与突触素共同分布，并显着促进EPSC。其次，我们证明这些受体参与了胆碱能活性对嗜铬细胞之间间隙连接偶联所施加的强音抑制控制，这是由α-RgIA处理过的切片中延髓内荧光素黄扩散增加所证明的。第三，我们出乎意料地发现，含α9的nAChRs主要（> 70％）促成冷应激大鼠乙酰胆碱诱导的电流，而α3nAChRs是无应激动物的主要促成途径。一致地，在冷应激大鼠中α9nAChR转录物和蛋白质的表达水平过表达。作为功​​能上的相关性，我们建议上调含α9的nAChR通道并在胆碱能信号传导中占主导地位，这可能是肾上腺髓质组织适当适应在压力情况下发生的内脏神经放电的机制之一。

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