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作 者:黄华玉[1]
机构地区:[1]中国科学院上海生理研究所
出 处:《神经科学》1995年第1期1-6,共6页Chinese Journal of Neuroscience
摘 要:大鼠海马脑片用[3H]去甲肾上腺素([3H]NA)孵育后,用无钙含2mmol/LEGTA任氏液灌流,用电刺激或高K+诱发[3H]NA释放。电刺激诱发的[3H]NA释放被TTX有力地抑制,被BAPTA—AM显著地减弱,但TTX和BAPTA—AM对高K+诱发的[3H]NA释放无作用。电刺激和高K+诱发的[3H]NA释放均被蛋白激酶C(PKC)的激活剂佛波醇脂加强,并被α2-自身受体激动剂clonidine所削弱。结果提示:在胞外无钙时,电刺激诱发海马脑片释放[3H]NA是来自囊泡的胞吐;Na+进入神经末梢和内Ca2+释放参与这一诱发释放过程,但不参与高K+诱发[3H]NA释放机制。The hippocampal slices preincubated with [3H]noradrenaline ([3H]NA) were superfused with Ca2+ -free medium containing 2 mmol/L EGTA and stimulated by electrical field stimulation or high K+. The electrically evoked [3H]NA release was inhibited potently by TTX and significantly by Ca2+ chelator, tetraacetoxy methyl ester of 1-2-bis - (2 -aminopenoxy) ethane -N, N, N', N' tetraacetic acid (BAPTA -AM), whereas TTX and BAPTA-AM had no effect on K+-evoked [3H]NA release. Both the evoked [3H]NA release were enhanced by the activator of protein kinase C, 4β-phorbol 12,13 -dibutyrate and diminished by the agonist of α2 -autoreceptor, clonidine. The findings suggest that under extracellular Ca2+-free conditions electrical stimulation of hippocampal slices evokes exocytotic release of [3H]NA and that Na+ entry and the liberation of internal Ca2+ stores are involved in the release process, but not in that induced by high K+.
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