Department of Physiology, Kazan State Medical University, R-420012 Kazan, Russia.
Brain Res Bull. 2010 Apr 5;81(6):613-6. doi: 10.1016/j.brainresbull.2009.12.010. Epub 2010 Jan 4.
Calcium/calmodulin-dependent protein-kinase II (CaMKII) is a ubiquitous intracellular enzyme, which is implicated in learning and memory mechanisms in the central nervous system, however its contribution to peripheral cholinergic neurotransmission is not well characterized. This study evaluated the impact of CaMKII on the function of frog neuromuscular synapse using electrophysiological recordings. Application of the selective CaMKII inhibitor KN-93 (5 microM) did not significantly alter the parameters of evoked and spontaneous quantal acetylcholine release under low-frequency stimulation (0.03 Hz). KN-93, on the other hand, produced pronounced changes in short-term synaptic plasticity: particularly, KN-93 inhibits the second component of paired-pulse facilitation (interpulse intervals of 100 ms and longer) and strengthens the depression of synaptic transmission under high-frequency stimulation (50 Hz). These results imply that CaMKII plays an important role in presynaptic functions at the frog neuromuscular junction, and potentiates quantal acetylcholine release under high-frequency activity.
钙/钙调蛋白依赖性蛋白激酶 II（CaMKII）是一种普遍存在的细胞内酶，它与中枢神经系统的学习和记忆机制有关，但它对周围胆碱能神经递质传递的贡献尚未得到很好的描述。本研究使用电生理记录评估了 CaMKII 对青蛙神经肌肉突触功能的影响。选择性 CaMKII 抑制剂 KN-93（5μM）的应用并未显著改变低频刺激（0.03Hz）下诱发和自发量子乙酰胆碱释放的参数。然而，KN-93 对短期突触可塑性产生了明显的变化：特别是，KN-93 抑制了成对脉冲易化的第二个成分（脉冲间隔为 100ms 及更长），并增强了高频刺激（50Hz）下突触传递的抑制。这些结果表明，CaMKII 在青蛙神经肌肉接头的突触前功能中起着重要作用，并增强了高频活动下量子乙酰胆碱的释放。
