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Publication : β3 integrin is dispensable for conditioned fear and hebbian forms of plasticity in the hippocampus.

First Author  McGeachie AB Year  2012
Journal  Eur J Neurosci Volume  36
Issue  4 Pages  2461-9
PubMed ID  22748100 Mgi Jnum  J:207656
Mgi Id  MGI:5559290 Doi  10.1111/j.1460-9568.2012.08163.x
Citation  McGeachie AB, et al. (2012) beta3 integrin is dispensable for conditioned fear and hebbian forms of plasticity in the hippocampus. Eur J Neurosci 36(4):2461-9
abstractText  Integrins play key roles in the developing and mature nervous system, from promoting neuronal process outgrowth to facilitating synaptic plasticity. Recently, in hippocampal pyramidal neurons, beta3 integrin (ITGbeta3) was shown to stabilise synaptic AMPA receptors (AMPARs) and to be required for homeostatic scaling of AMPARs elicited by chronic activity suppression. To probe the physiological function for ITGbeta3-dependent processes in the brain, we examined whether the loss of ITGbeta3 affected fear-related behaviours in mice. ITGbeta3-knockout (KO) mice showed normal conditioned fear responses that were similar to those of control wild-type mice. However, anxiety-like behaviour appeared substantially compromised and could be reversed to control levels by lentivirus-mediated re-expression of ITGbeta3 bilaterally in the ventral hippocampus. In hippocampal slices, the loss of ITGbeta3 activity did not compromise hebbian forms of plasticity--neither acute pharmacological disruption of ITGbeta3 ligand interactions nor genetic deletion of ITGbeta3 altered long-term potentiation (LTP) or long-term depression (LTD). Moreover, we did not detect any changes in short-term synaptic plasticity upon loss of ITGbeta3 activity. In contrast, acutely disrupting ITGbeta1-ligand interactions or genetic deletion of ITGbeta1 selectively interfered with LTP stabilisation whereas LTD remained unaltered. These findings indicate a lack of requirement for ITGbeta3 in the two robust forms of hippocampal long-term synaptic plasticity, LTP and LTD, and suggest differential roles for ITGbeta1 and ITGbeta3 in supporting hippocampal circuit functions.
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