Decreases in CaMKII activity trigger persistent potentiation of intrinsic excitability in spontaneously firing vestibular nucleus neurons.

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

Neuron

journal_title

Neuron

authors

Nelson AB,Gittis AH,du Lac S

doi

10.1016/j.neuron.2005.04.009

subject

Has Abstract

pub_date

2005-05-19 00:00:00

pages

623-31

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(05)00345-4

journal_volume

46

pub_type

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