Abstract:
:Calcium/calmodulin-dependent protein kinase II (CaMKII) has been described as a biochemical switch that is turned on by increases in intracellular calcium to mediate synaptic plasticity. Here, we show that reductions in CaMKII activity trigger persistent increases in intrinsic excitability. In spontaneously firing vestibular nucleus neurons, CaMKII activity is near maximal, and blockade of CaMKII activity increases excitability by reducing BK-type calcium-activated potassium currents. Firing rate potentiation, a form of plasticity in which synaptic inhibition induces long-lasting increases in excitability, is occluded by prior blockade of CaMKII and blocked by addition of constitutively active CaMKII. Reductions in CaMKII activity are necessary and sufficient to induce firing rate potentiation and may contribute to motor learning in the vestibulo-ocular reflex.
journal_name
Neuronjournal_title
Neuronauthors
Nelson AB,Gittis AH,du Lac Sdoi
10.1016/j.neuron.2005.04.009subject
Has Abstractpub_date
2005-05-19 00:00:00pages
623-31issue
4eissn
0896-6273issn
1097-4199pii
S0896-6273(05)00345-4journal_volume
46pub_type
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