Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Prog Mol Biol Transl Sci. 2014;122:61-87. doi: 10.1016/B978-0-12-420170-5.00003-9.
Learning and memory is widely believed to result from changes in connectivity within neuronal circuits due to synaptic plasticity. Work over the past two decades has shown that Ca(2+) influx during LTP induction triggers the activation of CaMKII in dendritic spines. CaMKII activation results in autophosphorylation of the kinase rendering it constitutively active long after the Ca(2+) dissipates within the spine. This "molecular switch"(1) mechanism is essential for LTP and learning and memory. Here, we discuss this key regulatory mechanism and the diversity of downstream targets that can be modulated by CaMKII to exert dynamic control of synaptic structure and function.
学习和记忆被广泛认为是由于神经元回路连接性的改变而产生的，这种改变是由于突触可塑性所致。过去二十年的工作表明，LTP 诱导过程中 Ca(2+)内流会触发树突棘中 CaMKII 的激活。CaMKII 的激活导致激酶的自身磷酸化，使其在 Ca(2+)在棘突内消散后很长时间内保持组成型活性。这种“分子开关”（1）机制对于 LTP 和学习记忆是必不可少的。在这里，我们讨论了这个关键的调节机制，以及 CaMKII 可以调节的下游靶标的多样性，以对突触结构和功能进行动态控制。
