Building stronger synapses: investigation of the structural role of CaMKII in long-term potentiation

神经元之间突触连接的长时程增强(LTP)是学习和记忆的基本机制。在大多数突触中，高度丰富的钙调非依赖性蛋白激酶II(CaMKII)通过将大量钙离子内流与突触后膜离子通道的磷酸化联系起来，发挥着至关重要的作用。除了它的酶作用外，CaMKII在LTP诱导过程中积累在树突棘中，在那里它建立了维持突触处于增强状态的分子相互作用。这个项目的目的是了解CaMKII如何通过结合化学、结构、生理和计算方法来发挥这一鲜为人知的后一种作用。

Long-term potentiation (LTP) of synaptic connections between neurons is a fundamental mechanism for learning and memory. In most synapses, highly abundant calmodulindependent protein kinase II (CaMKII) plays an essential role by linking large influxes of calcium to phosphorylation of ion channels embedded in the postsynaptic membrane. In addition to its enzymatic role, CaMKII accumulates in dendritic spines during LTP induction, where it establishes molecular interactions that maintain the synapse in a potentiated state. The aim of this project is to understand how CaMKII fulfils this poorly understood latter role by combining chemical, structural, physiological, and computational approaches.