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Titolo:
Activation of muscarinic receptors induces protein synthesis-dependent long-lasting depression in the perirhinal cortex
Autore:
Massey, PV; Bhabra, G; Cho, K; Brown, MW; Bashir, ZI;
Indirizzi:
Univ Bristol, Dept Anat, MRC, Ctr Synapt Plast, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 1, volume: 14, anno: 2001,
pagine: 145 - 152
SICI:
0953-816X(200107)14:1<145:AOMRIP>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
METABOTROPIC GLUTAMATE RECEPTORS; VISUAL RECOGNITION MEMORY; HIPPOCAMPAL CA1 REGION; DHPG-INDUCED LTD; TERM POTENTIATION; RAT HIPPOCAMPUS; IN-VITRO; SYNAPTIC DEPRESSION; IMPAIRMENT; LESIONS;
Keywords:
acetylcholine; carbachol; LTD; muscarinic receptor; perirhinal cortex; rat; recognition memory; synaptic plasticity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Bashir, ZI Univ Bristol, Dept Anat, MRC, Ctr Synapt Plast, Univ Walk, Bristol BS8 1TD, Avon, England Univ Bristol Univ Walk Bristol Avon England BS8 1TD on, England
Citazione:
P.V. Massey et al., "Activation of muscarinic receptors induces protein synthesis-dependent long-lasting depression in the perirhinal cortex", EUR J NEURO, 14(1), 2001, pp. 145-152

Abstract

There is strong evidence that decrements in neuronal activation in perirhinal cortex when a novel stimulus is repeated provide a neural substrate of visual recognition memory. There is also strong evidence that muscarinic acetylcholine (ACh) receptors are involved in learning and memory. However, the mechanisms underlying neuronal decrements in the perirhinal cortex and the basis of ACh involvement in learning and memory are not understood. In an in vitro preparation of rat perirhinal cortex we now demonstrate that activation of ACh receptors by carbachol (CCh) produces long-lasting depression (LLD) of synaptic transmission that is dependent on muscarinic M1 receptor activation. Crucially, the induction of this form of LLD requires neitherN-methyl-d-aspartate receptor activation nor synaptic stimulation. CCh-induced LLD was not blocked by the protein kinase C inhibitors staurosporine or BIM, or by the protein phosphatase inhibitor okadaic acid. However, each of cyclopiazonic acid (an agent that depletes intracellular calcium stores)and anisomycin (an inhibitor of protein synthesis) significantly reduced the magnitude of CCh-induced LLD. These mechanisms triggered by muscarinic receptor activation could play a role in the induction and/or expression of certain forms of activity-dependent long-term depression in perirhinal cortex. An understanding of CCh-induced LLD may thus provide clues to the mechanisms underlying lasting neuronal decrements that occur in the perirhinal cortex and hence for neural substrates of visual recognition memory.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 22:00:19