Synaptic transmission is a complex process, dysregulation of which underlies several neurological conditions. Collapsin response mediator protein 2 (CRMP2) is a microtubule associated protein expressed ubiquitously in the central nervous system. Identified initially in the context of Semaphorin 3A (Collapsin) induced growth cone collapse, more recent findings revealed the involvement of CRMP2 in ion channel trafficking, kinesin-dependent axonal transport and maintenance of intracellular calcium homeostasis. CRMP2 is a synaptic protein, expressed at pre- and post-synaptic sites. Interactions with proteins such as N-methyl-D-aspartate receptors, syntaxin1A as well as voltage-gated calcium and sodium channels, suggest that CRMP2 may control both the electrical and chemical components of synaptic transmission. This short review will outline the known synaptic interactions of CRMP2 and illustrate its role in synaptic transmission, thereby introducing CRMP2 as a prospective target for the pathophysiological modulation of aberrant synaptic activity.

突触传递是一个复杂的过程，其失调是几种神经系统疾病的基础。胶原蛋白介导蛋白2（CRMP2）是在中枢神经系统中普遍表达的微管相关蛋白。最初是在Semaphorin 3A（Collapsin）诱导的生长锥塌陷的背景下确定的，最近的发现表明CRMP2参与离子通道运输，驱动蛋白依赖性轴突运输和细胞内钙稳态的维持。CRMP2是一种突触蛋白，在突触前和突触后位点表达。与蛋白质（例如N-甲基-D-天冬氨酸受体，syntaxin1A以及电压门控的钙和钠通道）的相互作用表明CRMP2可以控制突触传递的电和化学成分。