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Learn Mem. 2007 Sep 6;14(9):606-15. Print 2007 Sep.

Alpha3-integrins are required for hippocampal long-term potentiation and working memory.

Author information

1
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.

Abstract

Integrins comprise a large family of heterodimeric, transmembrane cell adhesion receptors that mediate diverse neuronal functions in the developing and adult CNS. Recent pharmacological and genetic studies have suggested that beta1-integrins are critical in synaptic plasticity and memory formation. To further define the role of integrins in these processes, we generated a postnatal forebrain and excitatory neuron-specific knockout of alpha3-integrin, one of several binding partners for beta1 subunit. At hippocampal Schaffer collateral-CA1 synapses, deletion of alpha3-integrin resulted in impaired long-term potentiation (LTP). Basal synaptic transmission and paired-pulse facilitation were normal in the absence of alpha3-integrin. Behavioral studies demonstrated that the mutant mice were selectively defective in a hippocampus-dependent, nonmatch-to-place working memory task, but were normal in other hippocampus-dependent spatial tasks. The impairment in LTP and working memory is similar to that observed in beta1-integrin conditional knockout mice, suggesting that alpha3-integrin is the functional binding partner for beta1 for these processes in the forebrain.

PMID:
17848500
PMCID:
PMC1994082
DOI:
10.1101/lm.648607
[Indexed for MEDLINE]
Free PMC Article

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