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KMID : 0043319950180030153
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Archives of Pharmacal Research
1995 Volume.18 No. 3 p.153 ~ p.158
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The Time Course of NMDA-and Kainate-induced cGMP Elevation and Glutamate Release in Cultured Neuron
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Oh Sei-Kwan
Shin Chang-Sik
Kim Hack-Seang
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Abstract
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The levels of extracellualr glutamate, intracellular and cGMP were determined for 1 h with the excitatory amino acids, N-methyl-D-aspartate (NMDA) or kainate in cultured cerebellar granule cells. Both NMDA and kainate produced a time-dependent release of glutamate, and kainate was more potent than NMDA in glutamate elevation. The elevation of extracellular glutamate was not purely governed by intracellular concentration. However, in opposite to the time-dependent elevation of glutamate, the elevation of cGMP by NMDA and kainate were at maximum level in short-time (1 min) incubation then remarkably decreased with longer incubation times. Post-applications (30 min after agonist) of EAA antagonist did not block EAAs-induced glutamate elevation. However, NMDA antagonist, phencyclidine (PCP), blocked NMDA-induced cGMP elevation at pre- or post-application, but kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), paradoxically augmented kainate-induced cGMP elevation for 1 h incubation. These results show that NMDA or kainate induces time-dependent elevations of extracellular glutamate, while the elevations of cGMP by these EAAs are remarkably decreased with longer incubation times. However, NMDA- arid kainate-indcued glutamate release was blocked by pre-application of each receptor antagonist but not by post-application while EAA-induced was blocked by post-application of antagonist. These observations suggest that EAA-induced elevation of is not parallel with elevation of glutamate release or cGMP.
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KEYWORD
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Excitatory amino acids, NMDA, Kainate, cGMP, Ca++ influx
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