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首页> 外文期刊>Neuron >Decreases in CaMKII activity trigger persistent potentiation of intrinsic excitability in spontaneously firing vestibular nucleus neurons.
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Decreases in CaMKII activity trigger persistent potentiation of intrinsic excitability in spontaneously firing vestibular nucleus neurons.

机译:CaMKII活性的降低会触发自发激发前庭核神经元的内在兴奋性的持续增强。

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摘要

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.
机译:钙/钙调蛋白依赖性蛋白激酶II(CaMKII)被描述为一种生化开关,可通过增加细胞内钙来介导突触可塑性来开启。在这里,我们表明,CaMKII活性的降低会触发内在兴奋性的持续增加。在自发激发前庭核神经元中,CaMKII活性接近最大,并且通过降低BK型钙激活的钾电流,CaMKII活性的阻断增加了兴奋性。点火速率增强是可塑性的一种形式,其中突触抑制引起兴奋性的持久性提高,但由于事先阻断了CaMKII而被阻断,而加入了组成型活性CaMKII则阻止了这种作用。 CaMKII活性的降低是必要的,并且足以诱导射击频率增强,并且可能有助于前庭眼反射的运动学习。

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