title: Different modulation of cholinergic neuronal systems by dynorphin A (1-13) in carbon monoxide-exposed mice.
abstract: The effects of dynorphin A (1-13), a kappa-opioid receptor agonist, on the content of acetylcholine (ACh) and high K+-induced release of endogenous ACh were studied in mice exposed to carbon monoxide (CO). Mice were exposed to CO 3 times at 1-hr intervals and used 7 days after CO exposure. Administration of dynorphin A (1-13) (1.5 and 5.0 nmol/mouse, intracerebroventricularly) 15 min before killing significantly increased the ACh content in the striatum and hippocampus of control mice, but had no effect on the ACh content in CO-exposed mice. Dynorphin A (1-13) did not change the choline acetyltransferase (EC 2.3.1.6) activity in control or CO-exposed mice. The high K+-induced endogenous ACh release from hippocampal slices in CO-exposed mice was significantly lower than that of controls, although exposure to CO did not affect the basal release of endogenous ACh from hippocampal slices compared with controls. Dynorphin A (1-13) caused dose-dependent decreases in high K+-induced release of endogenous ACh from hippocampal slices in control mice. This inhibitory effect of dynorphin A (1-13) was blocked by co-perfusion with nor-binaltorphimine, a selective K-opioid receptor antagonist. On the other hand, dynorphin A (1-13) did not decrease high K+-induced release of endogenous ACh from hippocampal slices in CO-exposed mice. These results suggest that dysfunction of the cholinergic system occurred after exposure to CO, and as a result the inhibitory effects of dynorphin A (1-13) may be blocked in CO-exposed mice.
authors.affiliation: Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Meijo University, Nagoya, Japan. mhiramt@meijo-u.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Hiramatsu
authors.forename: M
authors.initials: M
authors.lastname: Murai
authors.forename: T
authors.initials: T
authors.lastname: Kameyama
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002248:Carbon Monoxide / Q000494:pharmacology*; D002794:Choline / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D002799:Cholinergic Fibers / Q000187:drug effects*; D004399:Dynorphins / Q000494:pharmacology*; D006624:Hippocampus / Q000378:metabolism; D008297:Male; D051379:Mice; D010446:Peptide Fragments / Q000494:pharmacology*; D011189:Potassium Chloride / Q000378:metabolism
chemical_list: D000701:Analgesics, Opioid; D010446:Peptide Fragments; D011189:Potassium Chloride; C026843:dynorphin (1-13); D004399:Dynorphins; D002248:Carbon Monoxide; D002795:Choline O-Acetyltransferase; D002794:Choline; D000109:Acetylcholine; D002118:Calcium