Present address: Department of Neuroscience and Brain Technologies, Italian Institute of Technology, Genova 16163, Italy.
β3 integrin is dispensable for conditioned fear and Hebbian forms of plasticity in the hippocampus
Article first published online: 2 JUL 2012
© 2012 The Authors. European Journal of Neuroscience © 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 36, Issue 4, pages 2461–2469, August 2012
How to Cite
McGeachie, A. B., Skrzypiec, A. E., Cingolani, L. A., Letellier, M., Pawlak, R. and Goda, Y. (2012), β3 integrin is dispensable for conditioned fear and Hebbian forms of plasticity in the hippocampus. European Journal of Neuroscience, 36: 2461–2469. doi: 10.1111/j.1460-9568.2012.08163.x
- Issue published online: 20 AUG 2012
- Article first published online: 2 JUL 2012
- Received 07 February 2012, revised 12 April 2012, accepted 13 April 2012
- hippocampal pyramidal neuron;
- long-term depression;
- long-term potentiation;
- synapse adhesion
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.