Ramade F, Baylé J D
Department of Endocrine Neurobiology, University of Montpellier, France.
Neuroendocrinology. 1989 Aug;50(2):165-9. doi: 10.1159/000125216.
The role of diencephalic cholinergic neurotransmission in regulating hypothalamic-pituitary-adrenocortical (HPA) axis was investigated by means of administration of hemicholinium-3 (HC-3), a blocker of acetylcholine synthesis, in the third ventricle of hemispherectomized pigeons. Except for an early increase in ACTH and corticosterone levels following injection as a bolus of HC-3 that was ascribed to some stress-like situation, all data indicated that hypothalamic acetylcholine depletion resulted in inhibiting effects on the HPA axis. Twenty-four hours after injection of 6 micrograms of HC-3, the response to acute stress was markedly reduced in both magnitude and duration. Permanent instillation of HC-3 in the third ventricle at the rate of 0.25 microgram/h for 9 days led to lowered basal resting HPA activity and severely affected the development of adaptation to chronic intermittent stress. The anticipatory conditioned, endocrine response did not appear whereas attenuation of the poststress component was amplified. It is suggested that cholinergic mechanisms are involved in modulating the HPA function and particularly the conditioning process that takes place in the course of adaptation of the HPA response to chronic intermittent application of the same stressor.
通过在大脑半球切除的鸽子第三脑室注射半胱氨酸-3（HC-3，一种乙酰胆碱合成阻滞剂），研究了间脑胆碱能神经传递在调节下丘脑-垂体-肾上腺皮质（HPA）轴中的作用。除了注射大剂量HC-3后促肾上腺皮质激素（ACTH）和皮质酮水平早期升高（归因于某种类似应激的情况）外，所有数据均表明下丘脑乙酰胆碱耗竭对HPA轴产生抑制作用。注射6微克HC-3后24小时，对急性应激的反应在幅度和持续时间上均显著降低。以0.25微克/小时的速率在第三脑室持续滴注HC-3 9天，导致基础静息HPA活性降低，并严重影响对慢性间歇性应激的适应能力发展。预期性条件内分泌反应未出现，而应激后成分的减弱被放大。提示胆碱能机制参与调节HPA功能，尤其是在HPA反应适应慢性间歇性施加相同应激源过程中发生的条件化过程。
