| First Author | Vitureira N | Year | 2011 |
| Journal | Nat Neurosci | Volume | 15 |
| Issue | 1 | Pages | 81-9 |
| PubMed ID | 22138644 | Mgi Jnum | J:180318 |
| Mgi Id | MGI:5306093 | Doi | 10.1038/nn.2995 |
| Citation | Vitureira N, et al. (2012) Differential control of presynaptic efficacy by postsynaptic N-cadherin and beta-catenin. Nat Neurosci 15(1):81-9 |
| abstractText | N-cadherin is a homophilic adhesion protein that remains expressed at mature excitatory synapses beyond its developmental role in synapse formation. We investigated the trans-synaptic activity of N-cadherin in regulating synapse function in rodent cultured hippocampal neurons using optical methods and electrophysiology. Interfering with N-cadherin in postsynaptic neurons reduced basal release probability (p(r)) at inputs to the neuron, and this trans-synaptic impairment of release accompanied impaired vesicle endocytosis. Moreover, loss of the GluA2 AMPA-type glutamate receptor subunit, which decreased p(r) by itself, occluded the interference with postsynaptic N-cadherin. The loss of postsynaptic N-cadherin activity, however, did not affect the compensatory upregulation of p(r) induced by chronic activity silencing, whereas postsynaptic beta-catenin deletion blocked this presynaptic homeostatic adaptation. Our findings suggest that postsynaptic N-cadherin helps link basal pre- and postsynaptic strengths to control the p(r) offset, whereas the p(r) gain adjustment requires a distinct trans-synaptic pathway involving beta-catenin. |
