Morphological plasticity of dendritic spines and synapses is thought to be crucial for their physiological functions. Here we show that αN-catenin, a linker between cadherin adhesion receptors and the actin cytoskeleton, is essential for stabilizing dendritic spines in rodent hippocampal neurons in culture. In the absence of αN-catenin, spine heads were abnormally motile, actively protruding filopodia from their synaptic contact sites. Conversely, αN-catenin overexpression in dendrites reduced spine turnover, causing an increase in spine and synapse density. Tetrodotoxin (TTX), a neural activity blocker, suppressed the synaptic accumulation of αN-catenin, whereas bicuculline, a GABA antagonist, promoted it. Furthermore, excess αN-catenin rendered spines resistant to the TTX treatment. These results suggest that αN-catenin is a key regulator for the stability of synaptic contacts.
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