Wang Zhao-Wen
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3401, USA.
Mol Neurobiol. 2008 Oct;38(2):153-66. doi: 10.1007/s12035-008-8039-7. Epub 2008 Aug 29.
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and the BK channel are enriched at the presynaptic nerve terminal, where CaMKII associates with synaptic vesicles whereas the BK channel colocalizes with voltage-sensitive Ca(2+) channels in the plasma membrane. Mounting evidence suggests that these two proteins play important roles in controlling neurotransmitter release. Presynaptic BK channels primarily serve as a negative regulator of neurotransmitter release. In contrast, presynaptic CaMKII either enhances or inhibits neurotransmitter release and synaptic plasticity depending on experimental or physiological conditions and properties of specific synapses. The different functions of presynaptic CaMKII appear to be mediated by distinct downstream proteins, including the BK channel.
钙/钙调蛋白依赖性蛋白激酶II（CaMKII）和大电导钙激活钾通道（BK通道）在突触前神经末梢高度富集，在那里CaMKII与突触小泡相关联，而BK通道则与质膜中的电压敏感钙通道共定位。越来越多的证据表明，这两种蛋白在控制神经递质释放中发挥重要作用。突触前BK通道主要作为神经递质释放的负调节因子。相比之下，突触前CaMKII根据实验或生理条件以及特定突触的特性，既可以增强也可以抑制神经递质释放和突触可塑性。突触前CaMKII的不同功能似乎由包括BK通道在内的不同下游蛋白介导。
