Assadian H, Ishikawa Y, Shimatsu A, Tanoh T, Imura H
Department of Internal Medicine, Kyoto University Faculty of Medicine, Japan.
J Auton Nerv Syst. 1991 Sep;35(3):193-8. doi: 10.1016/0165-1838(91)90097-m.
Intrathecal administration of thyrotropin-releasing hormone (TRH) resulted in an increase in plasma epinephrine (E) and glucose levels in conscious rats. To elucidate the mechanisms by which TRH stimulates the release of E, the animals were pretreated with 5,7-dihydroxytryptamine, parachlorophenylalanine, methysergide or ketanserin. Serotoninergic denervation suppressed the TRH-induced increase in plasma E and glucose levels, whereas inhibition of serotonin (5-HT) synthesis or blockade of 5-HT receptors did not suppress the responses. These findings suggest that the serotoninergic neurons, but not 5-HT itself, are involved in stimulating the sympathetic outflow by TRH at the spinal level.
鞘内注射促甲状腺激素释放激素（TRH）可导致清醒大鼠血浆肾上腺素（E）和葡萄糖水平升高。为了阐明TRH刺激E释放的机制，对动物进行了5,7-二羟色胺、对氯苯丙氨酸、麦角酰二乙胺或酮色林预处理。5-羟色胺能去神经支配抑制了TRH诱导的血浆E和葡萄糖水平升高，而抑制5-羟色胺（5-HT）合成或阻断5-HT受体并未抑制这些反应。这些发现表明，5-羟色胺能神经元而非5-HT本身参与了TRH在脊髓水平刺激交感神经输出的过程。
