| First Author | Chan CS | Year | 2007 |
| Journal | Learn Mem | Volume | 14 |
| Issue | 9 | Pages | 606-15 |
| PubMed ID | 17848500 | Mgi Jnum | J:147820 |
| Mgi Id | MGI:3842255 | Doi | 10.1101/lm.648607 |
| Citation | Chan CS, et al. (2007) Alpha3-integrins are required for hippocampal long-term potentiation and working memory. Learn Mem 14(9):606-15 |
| abstractText | 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. |
