[The clinical test in oral surgery of a new analgesic agent Y-3643 (2-amino-3 ethoxycarbonyl-4, 5, 6, 7-tetrahydrothieno-2, 3 cc-pyridine hydrochloride)].
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Biomedical subjects
Publications and source records attributed to S Kitayama.
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This commentary elaborates on the basic thesis developed by Rothbaum, Pott, Azuma, Miyake, and Weisz and underscores the significance of the co-constructive process of the self and social relationship. Implications for future cultural psychological inquiry in this area are discussed.
Effects of benzodiazepines were investigated on the gamma-aminobutyric acid-induced modulation of the basal and veratridine-evoked catecholamine release from cultured bovine adrenal chromaffin cells. GABA by itself, caused catecholamine release and facilitated veratridine-evoked catecholamine release. Midazolam enhanced the GABA-evoked catecholamine release in a dose-related fashion and further facilitated the enhancement by GABA of the veratridine-evoked catecholamine release. Clonazepam, a selective central-type benzodiazepine receptor agonist, also enhanced the GABA-induced catecholamine release, whereas ethyl-beta-carboline-3-carboxylate, an inverse agonist of the benzodiazepine receptor, reduced the GABA-evoked catecholamine release. The dose-response curve of the GABA-evoked catecholamine release was shifted to the left by midazolam without affecting the maximal response to GABA. Facilitation by midazolam and clonazepam of the GABA action or inhibition by ethyl-beta-carboline-3-carboxylate was antagonized by RO15-1788, which by itself had no effect on the basal or GABA- and veratridine-evoked catecholamine release. These results suggest that the central-type benzodiazepine receptor participates in the GABAergic modulation of the catecholamine release from adrenal chromaffin cells.