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Mild Traumatic Brain Injury Produces More Immediate and Prolonged Synaptic Plasticity Deficits in the Juvenile Female Hippocampus

Traumatic brain injury (TBI) is the leading cause of disability in individuals under 45 years of age, with mild TBI (mTBI) accounting for the majority of cases. The juvenile brain is in a period of robust synaptic reorganization and myelination, making adolescence a particularly vulnerable time to incur a TBI. Learning and memory deficits that involve the hippocampal formation are often observed following mTBI in adults. To examine this issue in the juvenile brain, we assessed changes in hippocampal synaptic plasticity following closed-head mTBI in male and female Long-Evans rats (25-28 days of age). Synaptic plasticity of field excitatory post-synaptic potentials (fEPSPs) was assessed using in vitro electrophysiology at either one hour, one day, seven days, or 28 days following mTBI in the dentate gyrus (DG) and the cornu ammonis area 1 (CA1) regions of the hippocampus. In female rats, the CA1 region ipsilateral to the impact showed a significant reduction in long-term potentiation (LTP) as early as one hour following mTBI. Similar LTP deficits were apparent at one day in the DG, and persisted to 28 days following injury. In male rats, a deficit in both DG- and CA1-LTP was maximal in the ipsilateral hemisphere by seven days following injury, but these deficits did not persist to 28 days post-injury. These data suggest that the juvenile brain is susceptible to mTBI-induced impairments in plasticity, and sex and regional differences are apparent in the expression and recovery of synaptic plasticity following mTBI. / Graduate

Identiferoai:union.ndltd.org:uvic.ca/oai:dspace.library.uvic.ca:1828/6051
Date29 April 2015
CreatorsWhite, Emily R.
ContributorsChristie, Brian R.
Source SetsUniversity of Victoria
LanguageEnglish
Detected LanguageEnglish
TypeThesis
RightsAvailable to the World Wide Web

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