Department of Neurophysiology, Graduate School of Medicine, Akita University, Akita, Japan.
Laboratory of Information Biology, Graduate School of Information Sciences Tohoku University, Sendai, Japan.
J Neurophysiol. 2020 Aug 1;124(2):443-457. doi: 10.1152/jn.00342.2019. Epub 2020 Jul 1.
Corticotropin-releasing hormone (CRH) is expressed in Barrington's nucleus (BarN), which plays an essential role in the regulation of micturition. To control the neural activities of BarN, glutamatergic and GABAergic inputs from multiple sources have been demonstrated; however, it is not clear how modulatory neurotransmitters affect the activity of BarN neurons. We have employed knock-in mice, CRH-expressing neurons of which are labeled with a modified yellow fluorescent protein (Venus). Using whole cell patch-clamp recordings, we examined the responses of Venus-expressing (putative CRH-expressing) neurons in BarN (Bar), as well as non-CRH-expressing neurons (Bar), following bath application of cholinergic agonists. According to the present study, the activity of Bar neurons could be modulated by dual cholinergic mechanisms. First, they are inhibited by a muscarinic receptor-mediated mechanism, most likely through the M2 subclass of muscarinic receptors. Second, Bar neurons are excited by a nicotinic receptor-mediated mechanism. Bar neurons also responded to cholinergic agents. Choline transporter-immunoreactive nerve terminals were observed in close proximity to the neurites, as well as the somata of Bar. The present results suggest that BarN neurons are capable of responding to cholinergic input. This study investigates the effects of bath-applied cholinergic agonists on Barrington's nucleus (BarN) neurons in vitro. They were either excitatory, through nicotinic receptors, or inhibitory, through muscarinic receptors. Putative corticotropin-releasing hormone (CRH)-expressing neurons in BarN, as well as putative non-CRH-expressing neurons, responded to cholinergic agonists.
促肾上腺皮质释放激素（CRH）表达在 Barrington 核（BarN）中，在调节排尿中起着至关重要的作用。为了控制 BarN 的神经活动，已经证明了来自多个来源的谷氨酸能和 GABA 能输入；然而，尚不清楚调节性神经递质如何影响 BarN 神经元的活性。我们使用了 CRH 表达神经元被修饰的黄色荧光蛋白（Venus）标记的基因敲入小鼠。通过全细胞膜片钳记录，我们研究了 Barrington 核（Bar）中 Venus 表达（假定的 CRH 表达）神经元以及非 CRH 表达神经元（Bar）在浴应用胆碱能激动剂后的反应。根据本研究，Bar 神经元的活动可以通过双重胆碱能机制来调节。首先，它们受到毒蕈碱受体介导的机制的抑制，很可能是通过毒蕈碱受体的 M2 亚类。其次，Bar 神经元受到烟碱受体介导的机制的兴奋。Bar 神经元也对胆碱能药物有反应。胆碱转运蛋白免疫反应性神经末梢被观察到与 Bar 神经元的轴突和胞体紧密相邻。目前的结果表明，BarN 神经元能够对胆碱能输入作出反应。本研究调查了在体外施加的胆碱能激动剂对 Barrington 核（BarN）神经元的影响。它们通过烟碱受体产生兴奋，或者通过毒蕈碱受体产生抑制。BarN 中的推定促肾上腺皮质释放激素（CRH）表达神经元以及推定非 CRH 表达神经元对胆碱能激动剂有反应。
