Involvement of α1-but Not α2-Adrenergic Systems in the Antagonizing Effect of Paeoniflorin on Scopolamine-Induced Deficit in Radial Maze Performance in Rats
Author(s) -
Hiroyuki Ohta,
Kinzo Matsumoto,
Takeshi Nabe,
Mineo Shimizu
Publication year - 1993
Publication title -
the japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.61.361
Subject(s) - paeoniflorin , yohimbine , prazosin , scopolamine , pharmacology , adrenergic , medicine , chemistry , endocrinology , chromatography , high performance liquid chromatography , antagonist , receptor
The effects of the novel calcium channel antagonist KB-2796, other calcium channel antagonists, an N-methyl-D-aspartate (NMDA) antagonist, non-NMDA antagonists, Mg2+, a Ca(2+)-chelator and a calcium channel agonist on neurotoxicity induced by a 10-min application of 100 microM glutamate were studied in rat hippocampal primary cell cultures. KB-2796 (0.1 and 1 microM), flunarizine (1 microM), nimodipine (10 microM), MK-801 (0.01-1 microM), Mg2+ (10 mM) and EGTA (10 mM) significantly prevented the neurotoxicity, but 6-cyano-7-nitro-quinoxalinedione (CNQX) (10 microM) and 6, 7-dinitro-quinoxalinedione (DNQX) (10 microM) did not. Bay K 8644 (10 and 100 nM) enhanced the neurotoxicity. These findings indicate that KB-2796 protects the neuronal cell from the glutamate-induced neurotoxicity, presumably by blocking the Ca2+ influx into brain neurons.
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