α-和β钙/钙调蛋白依赖性蛋白激酶II。受神经元活动的反向调节及其对突触强度的相反作用。
alpha- and betaCaMKII. Inverse regulation by neuronal activity and opposing effects on synaptic strength.
作者信息
Thiagarajan Tara C, Piedras-Renteria Erika S, Tsien Richard W
机构信息
Department of Molecular and Cellular Physiology, Beckman Center, Stanford University School of Medicine, Stanford, CA 94305, USA.
出版信息
Neuron. 2002 Dec 19;36(6):1103-14. doi: 10.1016/s0896-6273(02)01049-8.
We show that alpha and betaCaMKII are inversely regulated by activity in hippocampal neurons in culture: the alpha/beta ratio shifts toward alpha during increased activity and beta during decreased activity. The swing in ratio is approximately 5-fold and may help tune the CaMKII holoenzyme to changing intensities of Ca(2+) signaling. The regulation of CaMKII levels uses distinguishable pathways, one responsive to NMDA receptor blockade that controls alphaCaMKII alone, the other responsive to AMPA receptor blockade and involving betaCaMKII and possibly further downstream effects of betaCaMKII on alphaCaMKII. Overexpression of alphaCaMKII or betaCaMKII resulted in opposing effects on unitary synaptic strength as well as mEPSC frequency that could account in part for activity-dependent effects observed with chronic blockade of AMPA receptors. Regulation of CaMKII subunit composition may be important for both activity-dependent synaptic homeostasis and plasticity.
我们发现，α和β钙/钙调蛋白依赖性蛋白激酶II（CaMKII）在培养的海马神经元中受活性的反向调节：在活性增加时，α/β比值向α偏移，而在活性降低时向β偏移。该比值的变化幅度约为5倍，可能有助于使CaMKII全酶适应Ca(2+)信号强度的变化。CaMKII水平的调节使用不同的途径，一种途径对NMDA受体阻断有反应，单独控制αCaMKII，另一种途径对AMPA受体阻断有反应，涉及βCaMKII，并且可能涉及βCaMKII对αCaMKII的进一步下游效应。αCaMKII或βCaMKII的过表达对单突触强度以及微小兴奋性突触后电流（mEPSC）频率产生相反的影响，这可能部分解释了AMPA受体慢性阻断时观察到的活性依赖性效应。CaMKII亚基组成的调节对于活性依赖性突触稳态和可塑性可能都很重要。
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