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Electrogenesis Mechanisms of Slow Excitatory and Inhibitory Synaptic Potentials in Hamster Submandibular Ganglion Cells

仓鼠颌下神经节细胞慢兴奋性和抑制性突触电位的电发生机制

基本信息

批准号：
61570895
负责人：
TAKASHI Suzuki
金额：
$ 1.15万
依托单位：
Tokyo Dental College
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1987
项目状态：
已结题

项目摘要

In order to investigate the electrogenesis mechanisms of slow EPSP and slow IPSP in submandibular ganglion cell, bethanechol (BCh) was applied to the cells from micropipette using pressure injection system. The cellular responses corresponding to slow synapti potentials were recorded intracellularly from current- and volrage-clamped cells. BCh caused depolarizations in some cells and hyperpolarizations in ohters. The BCh hyperpolarization was caused by direct monosynaptic activation of muscarinic M_2 receptors accompanied by increased permeability of K+ ion. However, in mose cells, membrane input resistance (R_m) increased during BCh hyperolarization. The incidental mechanism, which increased Rm during BCh hyperpolarixation are still unclear. Calcium ions were indispensable in generation of BCh hyperpolatization. Although the existence of unknown receptor-operated Ca^<2+> channels was suggested, various blockers for voltage-dependent Ca^<2+> channels had no eddects on BCh hyperpolariza … More tion. Ca^<2+> ions released from endoplasmic retuculum after M_2 receptor activation might be partially involved in the generation of BCh hyperpolatization. The results supported the possibility that increased internal Ca^<2+> concentraion activates Ca^<2+>-activated K^+ channels in generation of BCh hyperpolarization. On the other hand, the BCh depolarization was caused by activation of M_1 receptors accompanied by decreased permeability of K^+ ion. The results suggested that M channels were mainly involved in generation of BCh depolarization. Introduction of the patch-clamp techniques was made to identify ion channels responsible for generation of slow PSPs in submandibular ganglion cells. In the first step, the parasympathetic neurons obtained from young hamster were cultered in a few days and conditions for culturing the cells were investigated. In the next step, the current of single maxitype Ca^<2+>-activated K^+ channel in cultered cell was tecorded from cell attached patch. The celluar responses were obtained by whole cell recording. The unsolved problem will be resolved in a further study using the improved techniqug. Less

为了探讨慢EPSP和慢IPSP在下颂神经节细胞中的电发生机制，采用压力注射系统，从微管中将氨甲酰胆碱（BCh）作用于下颂神经节细胞。慢突触电位对应的细胞反应记录在细胞内从电流和电压钳位的细胞。BCh引起部分细胞去极化和部分细胞超极化。BCh超极化是由M_2受体的直接单突触激活和K ~+通透性增加引起的。但在大多数细胞中，膜输入电阻（R_m）在BCh超极化过程中增加。在BCh超极化过程中增加Rm的偶然机制仍不清楚。钙离子在BCh超极化过程中是必不可少的。尽管存在未知的受体操纵的Ca^<2+>通道，但电压依赖性Ca^<2+>通道的各种阻断剂对BCh超极化无影响。 ...更多信息是的。M_2受体激活后内质网释放的Ca^<2+>离子可能部分参与了BCh超极化的形成。这一结果支持了细胞内Ca^2+浓度升高激活Ca^2+激活的K^+通道，从而引起BCh超极化的可能性。另一方面，BCh去极化是由于M_1受体的激活和K^+离子通透性的降低引起的。结果提示M通道主要参与了BCh去极化的产生。介绍了膜片钳技术，以确定负责产生慢PSP的下颌神经节细胞的离子通道。在第一步中，在几天内培养从年轻仓鼠获得的副交感神经元，并研究培养细胞的条件。在细胞贴附膜片上记录单个最大型Ca^2+激活的K^+通道电流。细胞反应采用全细胞记录法。未解决的问题将在进一步的研究中使用改进的技术来解决。少