Abstract
The content of acetylcholine (ACh) in nerve terminals or the dorsal hippocampus was examined after intraventricular, intraseptal, or intrahippocampal administration of a variety of endorphin/corticotropin neuropeptides. beta-Lipotropin, alpha-endorphin, gamma-endorphin, alpha- melanotropin, beta-melanotropin, adrenocorticotropin-1–39 (ACTH1–39), and ACTH4–10 (1, 3, 10, or 30 micrograms each) did not affect levels of ACh in the hippocampus 30 min after injection into the lateral ventricle. beta-Endorphin, administered intraventricularly (1, 3, 10, or 30 micrograms) or intraseptally (1 microgram), increased levels of ACh, while ACTH1–24, injected similarly, decreased levels of the neurotransmitter. ACh concentrations remained unchanged after direct application of beta-endorphin or ACTH1–24 (1, 3, 10, of 30 micrograms each) into Ammon's horn. Acute unilateral transection of the fimbria/superior fornix resulted in a time-related decrease in hippocampal ACh concentrations. Levels of ACh did not change 1 hr after transection; however, concentrations of hippocampal ACh decreased significantly 1 d or 1 week after deafferentation. ACh levels in the contralateral hippocampus remained unaffected at all times tested. Fimbrial transection blocked fully both endorphin- and corticotropin- induced changes in hippocampal ACh after the neuropeptides were injected into the lateral ventricle or the septal region. Naloxone, which, after subcutaneous (1 mg/kg) or intraventricular (100 micrograms) injection alone, failed to change levels of hippocampal ACh, antagonized the effects of intraventricular or intraseptal beta- endorphin or ACTH1–24 or hippocampal ACh levels. The results suggest a site of endorphin/corticotropin receptor interaction at the level of cholinergic cell bodies in the septal region for regulating the activity of septohippocampal cholinergic neurons.