Pan L H, Gilbert F
Département d'Endocrinologie, Hôpital Maisonneuve-Rosemont, Montréal, Québec, Canada.
Psychoneuroendocrinology. 1993;18(2):123-30. doi: 10.1016/0306-4530(93)90063-q.
Both food intake and pituitary ACTH release respond to activation of serotonergic 5-HT1a receptors. However, the effects of the 5-HT1a agonist 8-OH-DPAT on these two paradigms are probably mediated by different mechanisms. Ten micrograms of 8-OH-DPAT were microinjected into the rat paraventricular nuclei (PVN) of the hypothalamus and elicited an elevation of plasma ACTH concentration, but did not change food consumption when compared with controls. On the other hand, microinjection of the same dose of 8-OH-DPAT into the rat dorsal raphé nucleus increased food intake, but failed to alter plasma ACTH levels. This suggests that, among its various possible mechanisms of action, 8-OH-DPAT induces an increase of food intake in rats by activating presynaptic 5-HT1a autoreceptors in the raphé nuclei, where most serotonergic fibers originate, while its effect on plasma ACTH concentration occurs through activation of postsynaptic 5-HT1a receptors in the PVN, where some serotonergic fibers terminate.
食物摄入和垂体促肾上腺皮质激素（ACTH）释放均对血清素能5-HT1a受体的激活产生反应。然而，5-HT1a激动剂8-羟基二苯丙氨酸（8-OH-DPAT）对这两种模式的影响可能是由不同机制介导的。将10微克的8-OH-DPAT微量注射到大鼠下丘脑室旁核（PVN）中，可引起血浆ACTH浓度升高，但与对照组相比，食物消耗量没有变化。另一方面，将相同剂量的8-OH-DPAT微量注射到大鼠中缝背核中会增加食物摄入量，但未能改变血浆ACTH水平。这表明，在其各种可能的作用机制中，8-OH-DPAT通过激活中缝核中的突触前5-HT1a自身受体来诱导大鼠食物摄入量增加，大多数血清素能纤维起源于此，而其对血浆ACTH浓度的影响则是通过激活PVN中的突触后5-HT1a受体来实现的，一些血清素能纤维在此终止。
