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

A. B. McGeachie, A. E. Skrzypiec, L. A. Cingolani, M. Letellier, R. Pawlak, Y. Goda
European Journal of Neuroscience. 2012-07-02; 36(4): 2461-2469
DOI: 10.1111/j.1460-9568.2012.08163.x

PubMed
Lire sur PubMed



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, β3 integrin (ITGβ3) 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 ITGβ3-dependent processes in the brain, we examined
whether the loss of ITGβ3 affected fear-related behaviours in mice.
ITGβ3-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 ITGβ3 bilaterally in the ventral
hippocampus. In hippocampal slices, the loss of ITGβ3 activity did not compromise
hebbian forms of plasticity–neither acute pharmacological disruption of ITGβ3
ligand interactions nor genetic deletion of ITGβ3 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 ITGβ3 activity. In contrast, acutely
disrupting ITGβ1-ligand interactions or genetic deletion of ITGβ1 selectively
interfered with LTP stabilisation whereas LTD remained unaltered. These findings
indicate a lack of requirement for ITGβ3 in the two robust forms of hippocampal
long-term synaptic plasticity, LTP and LTD, and suggest differential roles for
ITGβ1 and ITGβ3 in supporting hippocampal circuit functions.

© 2012 The Authors. European Journal of Neuroscience © 2012 Federation of
European Neuroscience Societies and Blackwell Publishing Ltd.

 


Auteurs Bordeaux Neurocampus