Wood P L, Cheney D L, Costa E
J Pharmacol Exp Ther. 1979 Apr;209(1):97-103.
The intraventricular injection of alpha-melanocyte-stimulating hormone (alpha-MSH), adrenocorticotrophic hormone (ACTH1--24) or somatostatin increases the acetylcholine turnover rate (TRACh) in the hippocampus of rats. Two to 3 weeks after surgical transection of the projections from the cingulum of the entorhinal cortex to the hippocampus the injections of these peptides can still activate hippocampal TRACh. alpha-MSH, ACTH1--24 and somatostatin also increase hippocampal TRACh when injected two to 3 hr after section of the fimbria. In contrast, the intraseptal administration of these peptides fails to change the hippocampal TRACh. The results suggest that the increase in hippocampal TRACh elicited by the three polypeptides may be caused by their interaction with receptors located in the hippocampus. Moreover, the data exclude the possibility that these peptide receptors may be located in septum or in other telencephalic areas that contain neurons projecting to the hippocampus. In addition, this study shows that the septal-hippocampal cholinergic pathway is necessary to elicit a specific stretching-yawning syndrome described by Ferrari et al. (Ann. N.Y. Acad. Sci. 104: 330--345, 1963) after injection of alpha-MSH or ACTH1--24.
向大鼠脑室内注射α-黑素细胞刺激素（α-MSH）、促肾上腺皮质激素（ACTH1-24）或生长抑素，可提高海马中的乙酰胆碱周转率（TRACh）。在将内嗅皮质扣带回至海马的投射进行手术横断后2至3周，注射这些肽仍可激活海马TRACh。在切断穹窿后2至3小时注射α-MSH、ACTH1-24和生长抑素，也能提高海马TRACh。相反，向隔区内注射这些肽未能改变海马TRACh。结果表明，这三种多肽引起的海马TRACh升高可能是由于它们与海马中的受体相互作用所致。此外，数据排除了这些肽受体可能位于隔区或其他含有投射至海马的神经元的端脑区域的可能性。此外，本研究表明，隔区-海马胆碱能通路对于注射α-MSH或ACTH1-24后引发Ferrari等人（《纽约科学院学报》104: 330-345, 1963）所描述的特定伸展-打哈欠综合征是必需的。
