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Titolo:
REVERSION OF MUSCARINIC AUTORECEPTOR AGONIST-INDUCED ACETYLCHOLINE DECREASE AND LEARNING IMPAIRMENT BY DYNORPHIN-A-(1-13), AN ENDOGENOUS KAPPA-OPIOID RECEPTOR AGONIST
Autore:
HIRAMATSU M; MURASAWA H; MORI H; KAMEYAMA T;
Indirizzi:
MEIJO UNIV,FAC PHARMACEUT SCI,DEPT CHEM PHARMACOL NAGOYA AICHI 468 JAPAN
Titolo Testata:
British Journal of Pharmacology
fascicolo: 5, volume: 123, anno: 1998,
pagine: 920 - 926
SICI:
0007-1188(1998)123:5<920:ROMAAA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED DELAYED AMNESIA; ALZHEIMERS-DISEASE; NEUROTRANSMITTER RELEASE; CEREBRAL-CORTEX; RAT-BRAIN; MEMORY; HIPPOCAMPUS; GALANIN; BINDING; SLICES;
Keywords:
DYNORPHIN A (1-13); KAPPA-OPIOID RECEPTOR AGONIST; CARBACHOL; MUSCARINIC AUTORECEPTOR; LEARNING AND MEMORY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
M. Hiramatsu et al., "REVERSION OF MUSCARINIC AUTORECEPTOR AGONIST-INDUCED ACETYLCHOLINE DECREASE AND LEARNING IMPAIRMENT BY DYNORPHIN-A-(1-13), AN ENDOGENOUS KAPPA-OPIOID RECEPTOR AGONIST", British Journal of Pharmacology, 123(5), 1998, pp. 920-926

Abstract

1 We investigated whether carbachol, a muscarinic receptor agonist, induces learning and memory impairment, and if so, dynorphin A (1-13), an endogenous kappa-opioid receptor agonist, ameliorates the impairment of learning and memory induced by carbachol, by use of a step-through type passive avoidance task. 2 Carbachol induced a dose-related dualresponse. Carbachol (1.66 pmol per rat) administered directly into the hippocampus significantly shortened the step-through latency, while lower (0.166 pmol per rat) and higher (16.6 pmol per rat) doses of carbachol did not induce learning or memory impairment. 3 Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) administered 5 min after carbachol injection significantly reversed carbachol-induced impairment of learning and memory. 4 Perfusion with carbachol (3 x 10(-4) M) significantly decreased acetylcholine release in the hippocampus during perfusion as determined by in vivo brain microdialysis. This decrease in acetylcholine release was suppressed by co-perfusion with a low dose of atropine (10(-7) M). 5 Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) immediately before carbachol perfusion completely blocked this decrease in extracellular acetylcholine concentration induced by carbachol. 6 These antagonistic effects of dynorphin A (1-13) were abolished by treatment with norbinaltorphimine (5.44 nmol per rat, i.c.v.), a selective kappa-opioid receptor antagonist, 5 min before dynorphin A (1-13) treatment. dynorphin A (1-13) treatment. 7 These results suggest that the neuropeptide dynorphin A (1-13) ameliorates the carbachol-induced impairment of learning and memory, accompanied by attenuation of the reductions is acetylcholine release which may be associated with dysfunction of presynaptic cholinergic neurones via kappa-opioid receptors.

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Documento generato il 26/09/20 alle ore 12:12:58