• 1 January 1979
    • journal article
    • research article
    • Vol. 209  (1) , 97-103
Abstract
The intraventricular injection of .alpha.-melanocyte-stimulating hormone (.alpha.-MSH), ACTH1-24 or somatostatin increases the acetylcholine turnover rate (TRACh) in the hippocampus of rats. The injections of these peptides can still activate hippocampal TRACh 2-3 wk after surgical transection of the projections from the cingulum or the entorhinal cortex to the hippocampus. .alpha.-MSH, ACTH1-24 and somatostatin increase hippocampal TRACh when injected 2-3 h after section of the fimbria. Intraseptal administration of peptides fails to change the hippocampal TRACh. Apparently the increase in hippocampal TRACh elicited by the 3 polypeptides may be due to their interaction with receptors located in the hippocampus. The peptide receptors are not located in septum or in other telencephalic areas that contain neurons projecting to the hippocampus. The septalhippocampal cholinergic pathway is necessary to elicit a specific stretching-yawning syndrome after injection of .alpha.-MSH or ACTH1-24.