Abstract:
:Experience is a powerful sculptor of developing neural connections. In the primary visual cortex (V1), cortical connections are particularly susceptible to the effects of sensory manipulation during a postnatal critical period. At the molecular level, this activity-dependent plasticity requires the transformation of synaptic depolarization into changes in synaptic weight. The molecule alpha calcium-calmodulin kinase type II (alphaCaMKII) is known to play a central role in this transformation. Importantly, alphaCaMKII function is modulated by autophosphorylation, which promotes Ca(2+)-independent kinase activity. Here we show that mice possessing a mutant form of alphaCaMKII that is unable to autophosphorylate show impairments in ocular dominance plasticity. These results confirm the importance of alphaCaMKII in visual cortical plasticity and suggest that synaptic changes induced by monocular deprivation are stored specifically in glutamatergic synapses made onto excitatory neurons.
journal_name
Neuronjournal_title
Neuronauthors
Taha S,Hanover JL,Silva AJ,Stryker MPdoi
10.1016/s0896-6273(02)00966-2subject
Has Abstractpub_date
2002-10-24 00:00:00pages
483-91issue
3eissn
0896-6273issn
1097-4199pii
S0896627302009662journal_volume
36pub_type
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