Cao Y J, Peng Y Y
Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637, USA.
Neuroscience. 1999;92(4):1511-21. doi: 10.1016/s0306-4522(99)00077-9.
In bullfrog sympathetic ganglia, the ryanodine-sensitive Ca2+ store and mitochondria modulate [Ca2+] within nerve terminals. We used caffeine (10 mM) and carbonyl cyanide m-chlorophenylhydrazone (10 microM) to assess how these Ca2+ stores affect release of a neuropeptide, luteinizing hormone-releasing hormone, from these nerve terminals. Release of luteinizing hormone-releasing hormone was evoked by electrical stimulation to presynaptic nerves and was monitored as a late slow excitatory postsynaptic potential in ganglionic neurons. Caffeine increased release of luteinizing hormone-releasing hormone similarly whether the release was evoked by 4 or 20 Hz stimulations (by 2.7 +/- 1.1- and 3.2 +/- 0.9-fold, mean +/- S.E.M., n = 27, respectively). Carbonyl cyanide m-chlorophenylhydrazone augmented release of luteinizing hormone-releasing hormone evoked by 4 Hz stimulation much more strongly (by 11.8 +/- 1.8-fold) than it increased the release evoked by 20 Hz stimulation (by 3.6 +/- 1.3-fold, n = 25). We detected spontaneous release of luteinizing hormone-releasing hormone as a slow hyperpolarization in response to a brief application of an antagonist to the receptors for luteinizing hormone-releasing hormone in 65% (34 of 52) and 39% (11 of 28) of the ganglionic B and C neurons, respectively. Caffeine increased spontaneous release of luteinizing hormone-releasing hormone by 2.3 +/- 0.7-fold (n = 6) whereas carbonyl cyanide m-chlorophenylhydrazone increased this release by 4.27- and 1.76-fold (n = 2). Facilitation of Ca2+ release from the intracellular store by caffeine and inhibition of mitochondrial Ca2+ removal by carbonyl cyanide m-chlorophenylhydrazone increased spontaneous as well as evoked release of luteinizing hormone-releasing hormone. Moreover, caffeine increments of evoked release did not depend on the firing frequency of the nerve whereas carbonyl cyanide m-chlorophenylhydrazone augmentations of evoked release strongly depended on the firing frequency.
在牛蛙交感神经节中，对ryanodine敏感的Ca2+储存库和线粒体调节神经末梢内的[Ca2+]浓度。我们使用咖啡因（10 mM）和羰基氰化物间氯苯腙（10 microM）来评估这些Ca2+储存库如何影响神经肽促黄体生成激素释放激素从这些神经末梢的释放。通过电刺激突触前神经诱发促黄体生成激素释放激素的释放，并将其作为神经节神经元中晚期缓慢兴奋性突触后电位进行监测。无论释放是由4 Hz还是20 Hz刺激诱发，咖啡因都会使促黄体生成激素释放激素的释放增加相似的倍数（分别为2.7±1.1倍和3.2±0.9倍，平均值±标准误，n = 27）。羰基氰化物间氯苯腙增强4 Hz刺激诱发的促黄体生成激素释放激素释放的作用比增强20 Hz刺激诱发的释放作用更强（11.8±1.8倍）（3.6±1.3倍，n = 25）。我们在65%（52个中的34个）和39%（28个中的11个）的神经节B和C神经元中，通过短暂应用促黄体生成激素释放激素受体拮抗剂检测到促黄体生成激素释放激素的自发释放，表现为缓慢的超极化。咖啡因使促黄体生成激素释放激素的自发释放增加2.3±0.7倍（n = 6），而羰基氰化物间氯苯腙使这种释放增加4.27倍和1.76倍（n = 2）。咖啡因促进细胞内储存库释放Ca2+以及羰基氰化物间氯苯腙抑制线粒体Ca2+的清除，增加了促黄体生成激素释放激素的自发释放和诱发释放。此外，咖啡因对诱发释放的增加不依赖于神经的放电频率，而羰基氰化物间氯苯腙对诱发释放的增强强烈依赖于放电频率。
