Plasticity in the Hippocampus, Neurogenesis and Drugs of Abuse

Abstract

Synaptic plasticity in the hippocampus assists with consolidation and storage of long-lasting memories. Decades of research has provided substantial information on the cellular and molecular mechanisms underlying synaptic plasticity in the hippocampus, and this review discusses these mechanisms in brief. Addiction is a chronic relapsing disorder with loss of control over drug taking and drug seeking that is caused by long-lasting memories of drug experience. Relapse to drug use is caused by exposure to context and cues associated with the drug experience, and is a major clinical problem that contributes to the persistence of addiction. This review also briefly discusses some evidence that drugs of abuse alter plasticity in the hippocampus, and that development of novel treatment strategies that reverse or prevent drug-induced synaptic alterations in the hippocampus may reduce relapse behaviors associated with addiction.

Keywords: CA1; CA3; Dentate Gyrus; NPCs; long-term potentiation.

Figure 1

Modified from [13]. Simplified schematic representing projections in the hippocampus with emphasis on the inter- and intra- hippocampal circuits. Schematic representation of the coronal view of the hippocampus region indicating the subregions of the hippocampus and their location within the hippocampus; CA, Cornu Ammonis; CA1, CA2 and DG. Trisynaptic circuitry in the hippocampus is indicated with axons from the entorhinal cortex projecting unidirectionally to the apical dendrites of the hippocampal DG, CA1 and CA3 neurons (perforant path projection); DG neurons project to the apical dendrites of the CA3 pyramidal neurons (mossy fiber projection); CA3 neurons project to the apical dendrites of the CA1 neurons (schaffer collateral projection). The CA1 neurons have bidirectional projections to and from the BLA. The BLA also sends projections to the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), bed nucleus of the stria terminalis (BNST) and central nucleus of the amygdala. The DG and CA1 also receive direct inputs from the medial septum (MS).