Investigating the effect of an actin-stabilizing agent on rodent spatial memory following sleep deprivation

Sleep loss is known to negatively impact memory consolidation, particularly for memory forms mediated by the hippocampus. However, the mechanisms by which sleep deprivation alters synaptic plasticity in the hippocampus has yet to be defined. Dendritic spines play an important role in the formation of new memories in the hippocampus. It has been previously demonstrated in rodents that sleep loss results in spatial memory deficits and is accompanied by a large reduction in spine density in the CA1 region of the hippocampus. Actin filaments comprise the major structural components in dendritic spines. Cofilin, an enzyme that depolymerizes filamentous actin, has been shown to be upregulated following five hours sleep deprivation. The present study assessed whether profilin, an enzyme responsible for polymerizing actin monomers, is down-regulated following brief sleep deprivation. Profilin activity was not found to be altered following sleep deprivation. To assess whether stabilizing actin prevented spatial memory deficits following sleep deprivation, the actin-stabilizing drug jasplakinolide (JASP) was injected into area CA1 immediately after training and preceding sleep deprivation. A hippocampal-dependent behavioral paradigm was used to assess spatial long-term memory in mice. Sleep deprived mice who received JASP did not show spatial memory deficits. However, vehicle-treated sleep deprived mice also did not show deficits. This study aimed to further elucidate the mechanisms by which sleep deprivation alters synaptic plasticity in the hippocampus