beta-Catenin regulates excitatory postsynaptic strength at hippocampal synapses.
The precise contribution of the cadherin-beta-catenin synapse adhesion complex in the functional and structural changes associated with the pre- and postsynaptic terminals remains unclear. Here we report a requirement for endogenous beta-catenin in regulating synaptic strength and dendritic spine morphology in cultured hippocampal pyramidal neurons. Ablating beta-catenin after the initiation of synaptogenesis in the postsynaptic neuron reduces the amplitude of spontaneous excitatory synaptic responses without a concurrent change in their frequency and synapse density. The normal glutamatergic synaptic response is maintained by postsynaptic beta-catenin in a cadherin-dependent manner and requires the C-terminal PDZ-binding motif of beta-catenin but not the link to the actin cytoskeleton. In addition, ablating beta-catenin in postsynaptic neurons accompanies a block of bidirectional quantal scaling of glutamatergic responses induced by chronic activity manipulation. In older cultures at a time when neurons have abundant dendritic spines, neurons ablated for beta-catenin show thin, elongated spines and reduced proportion of mushroom spines without a change in spine density. Collectively, these findings suggest that the cadherin-beta-catenin complex is an integral component of synaptic strength regulation and plays a basic role in coupling synapse function and spine morphology.
Okuda
Takashi
T
Medical Research Council Laboratory for Molecular Cell Biology and Cell Biology Unit, Department of Pharmacology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Yu
Lily M Y
LM
Cingolani
Lorenzo A
LA
Kemler
Rolf
R
Goda
Yukiko
Y
D000818:Animals; D002478:Cells, Cultured; D006624:Hippocampus / Q000502:physiology*; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D051381:Rats; D013569:Synapses / Q000502:physiology*; D051176:beta Catenin / Q000502:physiology*
D051176:beta Catenin