Abstract
The maintenance of spine and synapse number during development is critical for neuronal circuit formation and function. Here we show that δ-catenin, a component of the cadherin-catenin cell adhesion complex, regulates spine and synapse morphogenesis during development. Genetic ablation or acute knockdown of δ-catenin leads to increases in spine and synapse density, accompanied by a decrease in tetrodotoxin induced spine plasticity. Our results indicate that δ-catenin may mediate conversion of activity-dependent signals to morphological spine plasticity. The functional role of δ-catenin in regulating spine density does not require binding to cadherins, but does require interactions with PDZ domain-containing proteins. We propose that the perturbations in spine and synaptic structure and function observed after depletion of δ-catenin during development may contribute to functional alterations in neural circuitry, the cognitive deficits observed in mutant mice, and the mental retardation pathology of Cri-du-chat syndrome.
Original language | English (US) |
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Pages (from-to) | 5435-5442 |
Number of pages | 8 |
Journal | Journal of Neuroscience |
Volume | 29 |
Issue number | 17 |
DOIs | |
State | Published - Apr 29 2009 |
ASJC Scopus subject areas
- Neuroscience(all)