Enhanced ventral hippocampal synaptic transmission and impaired synaptic plasticity in a rodent model of alcohol addiction vulnerability.

It has long been appreciated that adolescence represents a uniquely vulnerable period when chronic exposure to stressors can precipitate the onset of a broad spectrum of psychiatric disorders and addiction in adulthood. However, the neurobiological substrates and the full repertoire of adaptations within these substrates making adolescence a particularly susceptible developmental stage are not well understood. Prior work has demonstrated that a rodent model of adolescent social isolation (aSI) produces robust and persistent increases in phenotypes relevant to anxiety/stressor disorders and alcohol addiction, including anxiogenesis, deficits in fear extinction, and increased ethanol consumption. Here, we used extracellular field recordings in hippocampal slices to investigate adaptations in synaptic function and synaptic plasticity arising from aSI. We demonstrate that this early life stressor leads to enhanced excitatory synaptic transmission and decreased levels of long-term potentiation at hippocampal Schaffer collateral-CA1 synapses. Further, these changes were largely confined to the ventral hippocampus. As the ventral hippocampus is integral to neurocircuitry that mediates emotional behaviors, our results add to mounting evidence that aSI has profound effects on brain areas that regulate affective states. These studies also lend additional support to our recent proposal of the aSI model as a valid model of alcohol addiction vulnerability.