Cocaine-induced Activity in the Rat Hippocampus Using Phmri

Introduction The hippocampus (HF) is known to be involved in episodic memory and this brain region has increasingly been linked to drug-seeking behaviour in rodent behavioral models of substance abuse. Cocaine is a drug of abuse that can alter the magnitude of long-term potentiation (LTP) in the CA1 region of the HF (1). LTP is a form of synaptic plasticity that is thought to underlie learning/memory mechanisms at the molecular and cellular levels of information processing in the neural network. The psychostimulant effects of cocaine are thought to primarily result from its ability to block monoamine reuptake, including dopamine (DA) reuptake. This action increases DA levels in the brain and DA is known to facilitate LTP of glutamatergic synapses in the HF. Thus, cocaine actions in the HF will potentially facilitate the “memories of addiction” that persist following drug exposure. In terms of anatomical organization (especially efferent connectivity), the HF can be divided into two distinct sectors: dorsal hippocampus (dHF) and ventral hippocampus (vHF) (2). These sectors are also known to be dissociable at the functional level, with the dHF involved with spatial/cognitive processing and the vHF more concerned with motivational states (3). The BOLD activation following cocaine administration in laboratory rats has been reported, including the HF signal (4-5). However, an assessment has not been reported for discriminating between the dHF vs. the vHF. Our current study investigates such temporal responses in these two sectors in urethane anesthetized rats following systemic cocaine administration.