Nelson Alexandra B, Gittis Aryn H, du Lac Sascha
Systems Neurobiology Laboratories, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Neuron. 2005 May 19;46(4):623-31. doi: 10.1016/j.neuron.2005.04.009.
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.
钙/钙调蛋白依赖性蛋白激酶II（CaMKII）被描述为一种生化开关，可通过细胞内钙的增加而开启，以介导突触可塑性。在此，我们表明CaMKII活性的降低会引发内在兴奋性的持续增加。在自发放电的前庭核神经元中，CaMKII活性接近最大值，而阻断CaMKII活性可通过减少BK型钙激活钾电流来增加兴奋性。放电率增强是一种可塑性形式，其中突触抑制会诱导兴奋性的持久增加，它会被先前对CaMKII的阻断所阻断，并被添加组成型活性CaMKII所阻断。CaMKII活性的降低对于诱导放电率增强是必要且充分的，并且可能有助于前庭眼反射中的运动学习。
