Coordinating Synaptic Signaling with CRMP2.

Abstract

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.