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KMID : 0360419940300030263
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Korean Journal of Pharmacology
1994 Volume.30 No. 3 p.263 ~ p.272
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A Study on the Post-Receptor Mechanism of Adenosine Receptor on Acetylcholine Release in the Rat Hippocampus
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Choi Bong-Kyu
Oh Jae-Hee
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Abstract
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Since it was been reported that the depolarization-induced ACh release is inhibited by activation of presynaptic heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic receptor on the ACh release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the receptor-mediated control of ACh release in this study. Slices from rat hippocampus were equilibrated with and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 , 2ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from , decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by , a selective antagonist. The responses to N-ethylmaleimide , a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. PDB , a specific protein kinase C (PKC) activator, increased, whereas PMB , a PKC inhibitor, decreased the evoked ACh-release, and the adenosine effects were not affected by these agents. Nifedipine , a blocker of dihydropyridine analogue, significantly inhibited the adenosine effect, but glibenclamide, a blocker, did not. Finally, 8-bromo cyclic AMP , a membrane-permeable analogue of cAMP, did not alter the ACh release, but adenosine effects were inhibited by pretreatment with large dose of 8-br-cAMP . These results indicate that the decrement of the evoked ACh-release by receptor is mediated by the G-protein, and nifedipine-sensitive and adenylate cyclase system are coupled partly to this effect, and that protein kinase C and glibenclamide-sensitive are not involved in this process.
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KEYWORD
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Hippocampus, release, Adenosine, cAMP
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