| Project/Area Number |
62480109
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Kurume University |
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Principal Investigator |
AKASU Takashi Kurume University School of Medicine Professor, 医学部, 教授 (60113213)
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| Co-Investigator(Kenkyū-buntansha) |
TOKIMASA Takayuki Kurume University School of Medicine Associate Professor, 医学部, 助教授 (50155511)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Modulation of synaptic transmission / Cholinergic neuron / Peptidergic neuron / Synaptic interaction / Sympathetic ganglia / Bullfrog / 受容体感受性促進 / シナプス伝達調節 / ウシ蛙交換神経節 / アセチルコリン / コリン性神経 / ペプタイド性神経 / コリン性伝達抑制 / 異シナプス性伝達調節 / コリン性伝達 / ペプタイド性伝達 / 受容体感受性 / ガンマアミノ酪酸 / セロトニン |
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| Research Abstract |
Pharmacological study has reported previously modulation of cholinergic transmission induced by interaction between nicotinic and peptidergic transmitter substances. However, there was considerable disagreement among the experimental findings. The purpose of the present study was to examine the existence of synaptic interaction between peptidergic and nicotinic postsynaptic responses in bullfrog sympathetic ganglia, using intracellular and voltage-clamp recording methods. Stimulations of both 3rd-5th (0.2 Hz) and 8th (30 Hz) spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of the fast EPSPs was decreased during the course of the late slow EPSP in a majority of neurons. The quantal content of the fast EPSP was also decreased. Acetylcholine-induced depolarization ACh potential and current (ACh current) produced by ionophoretic application of ACh were not changed or increased during th
… More
e late slow EPSP. Bath-application of luteinizing hormone-releasing hormone (LH-RH; 40 nM-4 M) depressed the fast EPSP in a concentration-dependent manner. At a concentration 1 M, LH-RH produced a 63 8 % depression of the quantal content of the fast EPSP. LH-RH depressed the frequency of the miniature EPSP. Antagonists for LH-RH receptor ([D-Phe^<2,6>, Pro^3]-LH-RH and [d-pGlu^1, D-Phe^2, D-Tri^<3,6> -LH-RH) prevented the presynaptic inhibition of the fast EPSP induced by LH-RH. These results suggest that the fast EPSP is depressed during the late slow EPSP by decreasing the evoked release of ACh from presynaptic nerve terminals in bullfrog sympathetic ganglia. In some sympathetic B neurons. LH-RH increased the ACh current and shifted the dose response curve in parallel to the left. Voltage-clamp analyses using a single sympathetic neurons showed that LH-RH did not change the properties of ion channels associated with the nicotinic receptor. LH-TH may facilitate the sensitivity of the nicotinic ACh receptors by increasing an affinity of ACh to the receptor. Less
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