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Impaired Synaptic Plasticity in a Rodent Model of Intimate Partner Violence-Related Brain Injury
Justin Brand1, Eric Eyolfson1, Kirsten R B Suesser1,2
1Neuroscience Program, School of Medical Sciences, University of Victoria, Victoria, British Columbia, Canada.
Abstract:
Intimate partner violence-related brain injury (IPV-BI) predominantly affects women and often reflects both structural trauma from mild traumatic brain injury (mTBI), as well as ischemia/hypoxia from non-fatal strangulation (NFS). This polytrauma can impair cognitive function, particularly learning and memory processes, which may contribute to the continuation of the cycle of violence. This study investigates the effects of mTBI and hypoxic/ischemic injury on hippocampal long-term potentiation (LTP), a biological model of learning and memory, to determine if the combination of mTBI+NFS would exacerbate deficits in LTP. Female rats were randomly assigned to either Sham, mTBI, NFS, or mTBI+NFS groups to assess acute injury metrics and LTP capacity 7 days after injury. At the time of injury, NFS and mTBI+NFS groups exhibited significant reductions in blood oxygen saturation, heart rate, and poor neurological assessment metrics. Isolated mTBI and NFS impaired LTP in the CA1 hippocampal region while mTBI+NFS increased synaptic excitability in the CA1 yet impaired CA1 LTP. Contrary to our hypothesis, the combined mTBI+NFS did not exacerbate deficits, but these findings highlight that even a single episode of mTBI or NFS is sufficient to impair hippocampal LTP in the female CA1 region.
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