Sherbourne C D, Gonzales R, Goldyne M E, Levine J D
School of Medicine, University of California, San Francisco 94143-0452.
Neurosci Lett. 1992 May 25;139(2):188-90. doi: 10.1016/0304-3940(92)90548-l.
The contribution of exocytosis to norepinephrine-stimulated prostaglandin release from sympathetic postganglionic neurons was evaluated in homogenates of adult rat superior cervical ganglia. Incubation of ganglion homogenates with norepinephrine (1 mM) for 30 min caused an increased release of prostaglandin E2 and prostaglandin I2 (measured as the stable metabolite, 6-keto-PGF1a). Neither tetrodotoxin (10 mM), K+ (120 mM), nor EDTA in Ca(2+)-free buffer affected prostaglandin generation under basal and norepinephrine-stimulated conditions. These results suggest that the increase in prostaglandin production by sympathetic neurons after norepinephrine administration is not through the release of previously synthesized intracellular stores. Instead, the increase in prostaglandins in response to norepinephrine appears to be explained by de novo synthesis.
在成年大鼠颈上神经节匀浆中评估了胞吐作用对去甲肾上腺素刺激的交感神经节后神经元前列腺素释放的贡献。将神经节匀浆与去甲肾上腺素（1 mM）孵育30分钟会导致前列腺素E2和前列腺素I2释放增加（以稳定代谢物6-酮-PGF1α测量）。在基础和去甲肾上腺素刺激条件下，河豚毒素（10 mM）、K⁺（120 mM）或无钙缓冲液中的乙二胺四乙酸均不影响前列腺素的生成。这些结果表明，去甲肾上腺素给药后交感神经元前列腺素产生的增加不是通过释放先前合成的细胞内储存物质。相反，对去甲肾上腺素反应中前列腺素的增加似乎可以用从头合成来解释。
