Electrogenesis Mechanisms of Slow Excitatory and Inhibitory Synaptic Potentials in Hamster Submandibular Ganglion Cells
| Project/Area Number |
61570895
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Tokyo Dental College |
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Principal Investigator |
TAKASHI Suzuki Tokyo Dental College, Associate Professor, 歯学部, 助教授 (10064669)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1987: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Submandibular ganglion / Slow excitatory postsynaptic potential / Slow inhibitory postsynaptic potential / Parasympathetic ganglin cell / Ion channel / Electrogenesis mechanism / Muscarinic receptor / ムスカリン様刺激薬 / 顎下神経節細胞 / 緩徐シナプス電位発現機序 / 電位固定法 / 【Ca^(2+)】活性化【K^+】チャンネル / Mチャンネル |
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| Research Abstract |
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
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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
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(2 results)
Research Products
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