Language

English

Publication Date

1-4-2006

Journal

The Journal of Neuroscience

DOI

10.1523/JNEUROSCI.4110-05.2006

PMID

16399691

PubMedCentral® Posted Date

January 2006

PubMedCentral® Full Text Version

Post-print

Abstract

Integrins comprise a large family of cell adhesion receptors that mediate diverse biological events through cell-cell and cell-extracellular matrix interactions. Recent studies have shown that several integrins are localized to synapses with suggested roles in synaptic plasticity and memory formation. We generated a postnatal forebrain and excitatory neuron-specific knock-out of beta1-integrin in the mouse. Electrophysiological studies demonstrated that these mutants have impaired synaptic transmission through AMPA receptors and diminished NMDA receptor-dependent long-term potentiation. Despite the impairment in hippocampal synaptic transmission, the mutants displayed normal hippocampal-dependent spatial and contextual memory but were impaired in a hippocampal-dependent, nonmatching-to-place working memory task. These phenotypes parallel those observed in animals carrying knock-outs of the GluR1 (glutamate receptor subunit 1) subunit of the AMPA receptor. These observations suggest a new function of beta1-integrins as regulators of synaptic glutamate receptor function and working memory.

Keywords

Animals, Antigens, CD29, Hippocampus, Memory, Mice, Mice, Inbred C57BL, Mice, Knockout, Neuronal Plasticity, Receptors, AMPA, Synaptic Transmission

Published Open-Access

yes

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