Gap Junction Communication in Memory Retrieval and Extinction of Cocaine Seeking

Abstract

Blocking drug-associated memory retrieval or enhancing extinction of drug-seeking behavior are two strategies that could limit relapse in drug addicts. The loci of retrieval and extinction memory processes include the prelimbic medial prefrontal cortex and the infralimbic medial prefrontal cortex, respectively. The neurochemical and synaptic mechanisms underlying drug-related behavior have received considerable attention, but extrasynaptic mechanisms are relatively unexplored. One form of cellular communication, gap junction communication, may play a role in drug-related learning and memory. Gap junction communication between neurons and astrocytes provide a cytoplasmic continuity between connected cells and both neuronal and astrocytic gap junction communication have been demonstrated to be involved with development and maintenance of the CNS, and also aversive and appetitive paradigms of learning. However, in retrieval or extinction of drug-seeking behavior, the role of gap junction communication is unknown. Here I describe a series of experiments that investigate astrocytic and neuronal gap junction communication in the retrieval and extinction of a cocaine conditioned place preference using microinfusions and confocal imaging.