Chemogenetic activation of the perirhinal cortex reverses methamphetamine-induced memory deficits and reduces relapse.

ABSTRACT: Prolonged use of methamphetamine (meth) has been associated with episodic memory deficits in humans, and preclinical rat models of meth self-administration indicate the memory deficits are a consequence of meth use. Others have suggested that the meth-induced memory deficits may promote a cyclical pattern of drug use, abstinence, and relapse, although preclinical evidence for this relationship is somewhat lacking. The memory deficits in preclinical models manifest as a loss of novel object recognition (NOR) memory. These deficits occur one to two weeks after cessation of meth use and involve the perirhinal cortex, a parahippocampal region essential to NOR memory. We hypothesized that a loss of perirhinal cortex function contributes to both the NOR memory deficits and increased vulnerabilit

SUBMITTER: Peters J 

PROVIDER: S-EPMC6097768 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature