Abstract
The precise contribution of the cadherin-β-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 β-catenin in regulating synaptic strength and dendritic spine morphology in cultured hippocampal pyramidal neurons. Ablating β-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 β-catenin in a cadherin-dependent manner and requires the C-terminal PDZ-binding motif of β-catenin but not the link to the actin cytoskeleton. In addition, ablating β-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 β-catenin show thin, elongated spines and reduced proportion of mushroom spines without a change in spine density. Collectively, these findings suggest that the cadherin-β-catenin complex is an integral component of synaptic strength regulation and plays a basic role in coupling synapse function and spine morphology.
Original language | English |
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Pages (from-to) | 13479-13484 |
Number of pages | 6 |
Journal | Proceedings of the National Academy of Sciences of the United States of America |
Volume | 104 |
Issue number | 33 |
DOIs | |
Publication status | Published - 2007 Aug 14 |
Externally published | Yes |
Keywords
- Quantal scaling
- Spine morphology
- Synapse adhesion proteins
- α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors
ASJC Scopus subject areas
- General