Abstract
Acetylcholine (1 and 50 mug), carbamylcholine (1 and 10 mug), and oxotremorine (10 mug) were infused into the 3rd ventricle of rats with deafferented medial basal hypothalamus (MBH); infusions failed to stimulate ACTH release as shown by the plasma corticosterone level. Implants of an atropine-fluorescein mixture (200-250 mug) inhibited the stress-induced rise of plasma corticosterone only when dye from the implant stained large portions of the median eminence and the basal hypothalamus. Atropine implants near the electrodes inhibited the rise in plasma corticosterone usually produced by electrical stimulation in the anterior hypothalamus. Atropine crystals or a 2% atropine sulphate solution placed on the median eminence blocked conduction of action potential in the hypothalamo neurohypophyseal and tubero-infundibular pathways. The evidence will be discussed for and against the participation of a cholinergic synapse (in the MBH) that activates ACTH release after stressful neural stimuli.
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