| Project/Area Number |
05640758
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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 |
動物生理・代謝
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| Research Institution | Hokkaido University |
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Principal Investigator |
TAKAHATA Masakazu Hokkaido Univ., Grad.Sch.Sci., Professor, 理学部, 教授 (10111147)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Crayfish / Nonspiking interneuron / Identified cell / Dendrite / Synaptic integration / Acetylcholine / Nicotinic agonist / Muscarinic agonist / 伝達物質 / 受容体 / 神経生理学 |
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| Research Abstract |
The LDS interneuron, a sensory nonspiking interneuron identified in the terminal abdominal ganglion of the crayfish Procambarus clarkii Girard, is monosynaptically exited by mechanosensory afferents on the side ipsilateral to its soma.Pharmacological characteristics of this synaptic transmission were studied by examining the sffects of acetylcholine (ACh) agonists on the synaptic response evoked by electrical stimulation of sensory afferents using intracellular recording techniques.
When ACh or its general agonist carbachol was applied by perfusion, the interneuron showed depolarization and the peak amplitude of the synaptic response was decreased.Current injection experiments confirmed that the decrease in the synaptic response was not due to the depolarization caused by the drug.Similar results were obtained by applying the drug under the low-Ca^<2+>, high Mg^<2+> condition.Both the membrane potential and the synaptic response returned to their original state after washing the prepara
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tion with normal saline.It is thus concluded that the dendritic membrane of the LDS interneuron possesses receptors for ACh.Application of TMA,a selective nicotinic agonist of ACh, also caused the membrane depolarization and a decrease of the synaptic response, whereas application of oxotremorine and other muscarinic agonists caused similar synaptic suppression but never elicited the membrane depolarization.The results suggest that ACh receptors the LDS interneuron resemble the nicotinic ACh receptors in their sensitivity to agonists and that the muscarrinic agonists suppress the synaptic transmission presumably through their presynaptic action.Voltage clamp experiments revealed that the half decay time of the synaptic current evoked by sensory stimulation was about 10msec.This short time course of the synaptic response seems to be based on the rapid action of ACh receptors on the LDS interneuron membrane which would work as the vertebrate nicotinic ACh receptors by opening the ionic channels in direct response to the transmitter molecules. Less
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