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机构地区:[1]中国科学院上海生理研究所
出 处:《中国药理学报》1994年第3期215-219,共5页Acta Pharmacologica Sinica
摘 要:在细胞外无钙时,佛波醇基酯能加强3,4-二氨基吡啶、藜芦定或哇巴因所诱发的去甲上腺素(NE)释放,但对莫能星(Mon)诱发的NE释放无作用。河豚毒素能阻断前3种物质诱发的NE释放,但对Mon诱发的释放无作用。钙整合剂BAPTA-AM能抑制这4种物质诱发的NE释放。结果提示蛋白激酶c仅调制由膜去极化因素诱发的NE释放。4β-Phorbol 12, 13-dibutyrate ( PDB ) enhanced [3H ] norepinephrine ([3H]NE) release from rat hippocampal slices evoked by 3, 4-diaminopyridine (3, 4-DAP, 100-400 nmol·L-1), veratridine (1 - 7 umol ·L-1) or ouabain (100 - 200 μmol·L-1), but had no effect on those evoked by monensin (0. 01 - 10 μmol·L-1) in the absence of extracellular Ca2+. Tetrodotoxin (TTX, 0. 3 μmol ·L-1) blocked [3H]NE release evoked by 3,4-DAP, veratridine, or ouabain, but failed to affect that evoked by monensin. Tetraace-toxy methyl ester of l-2-bis-( 2-amino-phenoxy) ethane-N,N ,N', N'-tetraacetic acid (BAPTA-AM), Ca2+ chelator, inhibited the [3H]NE release evoked by these substances, but did not inhibit the enhancement of the evoked NE release by PDB. The findings suggest that under external Ca2+-free conditions protein kinase C activation enhances [3H]NE release evoked by the membrane depolarizing agents, but does not affect that evoked by Na+-induced internal Ca2+ release.
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