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Titolo:
M-1 muscarinic acetylcholine receptors activate extracellular signal-regulated kinase in CA1 pyramidal neurons in mouse hippocampal slices
Autore:
Berkeley, JL; Gomeza, J; Wess, J; Hamilton, SE; Nathanson, NM; Levey, AI;
Indirizzi:
Emory Univ, Dept Neurol, WMB 6000, Atlanta, GA 30322 USA Emory Univ Atlanta GA USA 30322 t Neurol, WMB 6000, Atlanta, GA 30322 USA NIDDKD, NIH, Bethesda, MD 20892 USA NIDDKD Bethesda MD USA 20892NIDDKD, NIH, Bethesda, MD 20892 USA Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 ept Pharmacol, Seattle, WA 98195 USA
Titolo Testata:
MOLECULAR AND CELLULAR NEUROSCIENCE
fascicolo: 5, volume: 18, anno: 2001,
pagine: 512 - 524
SICI:
1044-7431(200111)18:5<512:MMARAE>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; PROTEIN-COUPLED RECEPTORS; METHYL-D-ASPARTATE; RAT HIPPOCAMPUS; MAP KINASE; KNOCKOUT MICE; TYROSINE KINASES; PC12 CELLS; PHOSPHORYLATION; PATHWAYS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Levey, AI Emory Univ, Dept Neurol, WMB 6000, 1639 Pierce Dr, Atlanta, GA 30322 USA Emory Univ 1639 Pierce Dr Atlanta GA USA 30322 nta, GA 30322 USA
Citazione:
J.L. Berkeley et al., "M-1 muscarinic acetylcholine receptors activate extracellular signal-regulated kinase in CA1 pyramidal neurons in mouse hippocampal slices", MOL CELL NE, 18(5), 2001, pp. 512-524

Abstract

Activation of extracellular signal-regulated kinases (ERK) Is crucial for many neural functions, including learning, memory, and synaptic plasticity. As muscarinic acetylcholine receptors (mAChR) modulate many of the same higher brain functions as ERK, we examined mAChR-mediated ERK activation in mouse hippocampal slices. The cholinergic agonist carbachol caused an atropine-sensitive ERK activation in the dendrites and somata CAI pyramidal neurons. To determine the responsible mAChR subtype, we combined pharmacologic and genetic approaches. Pretreatment with M-1 antagonists inhibited ERK activation. Furthermore, mAChR-induced ERK activation was absent in slices fromM-1 knockout mice. ERK activation was normal in slices derived from other mAChR subtype knockouts (M-2, M-3, and M-4), although these other subtypes are expressed in many of the same neurons. Thus, we demonstrate divergent functions for the different mAChR subtypes. We conclude that M-1 is responsible for mAChR-mediated ERK activation, providing a mechanism by which M-1 may modulate learning and memory.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 22:16:10