Primary blast injury erases long term potentiation in rat brain organotypic hippocampal slices

Traumatic brain injury (TBI) has been diagnosed in nearly 300,000 members of the US armed forces since 2000 [1]. Common symptoms of these injuries include concussion, loss of spatial navigation, behavior/mood changes and memory loss [2‐3]. Blast‐related TBI poses a significant problem for military personnel both in combat and in training. Primary blast loading, the blast loading caused by the interaction of the shock wave with the skull and brain tissue, remains poorly understood. Great emphasis has been placed on identifying operational thresholds for blast‐induced TBI. Previous studies have attempted to observe the effect of blast‐induced TBI on cognitive/behavioral changes in mice following exposure [4]. Another approach is to quantify alterations in electrophysiological activity within acute or cultured neurons/slices following blast [5]. These in vitro approaches may have utility for determining tolerance criteria to primary blast in terms of changes in neural function. This short communication investigates the effect of primary blast loading on multiple electrophysiological measures within rat brain organotypic hippocampal slice cultures (OHSCs).