Cognitive Impairment After Traumatic Brain Injury is Associated with Reduced Long-term Depression of Excitatory Postsynaptic Potential in the Rat Hippocampal Dentate Gyrus

Overview

Journal Neural Regen Res

Date 2018 Aug 24

PMID 30136690

Citations 6

Authors

Bao-Liang Zhang

Yue-Shan Fan

Ji-Wei Wang

Zi-Wei Zhou

Yin-Gang Wu

Meng-Chen Yang

Dong-Dong Sun

Jian-Ning Zhang

Affiliations

Soon will be listed here.

Abstract

Traumatic brain injury can cause loss of neuronal tissue, remote symptomatic epilepsy, and cognitive deficits. However, the mechanisms underlying the effects of traumatic brain injury are not yet clear. Hippocampal excitability is strongly correlated with cognitive dysfunction and remote symptomatic epilepsy. In this study, we examined the relationship between traumatic brain injury-induced neuronal loss and subsequent hippocampal regional excitability. We used hydraulic percussion to generate a rat model of traumatic brain injury. At 7 days after injury, the mean modified neurological severity score was 9.5, suggesting that the neurological function of the rats was remarkably impaired. Electrophysiology and immunocytochemical staining revealed increases in the slope of excitatory postsynaptic potentials and long-term depression (indicating weakened long-term inhibition), and the numbers of cholecystokinin and parvalbumin immunoreactive cells were clearly reduced in the rat hippocampal dentate gyrus. These results indicate that interneuronal loss and changes in excitability occurred in the hippocampal dentate gyrus. Thus, traumatic brain injury-induced loss of interneurons appears to be associated with reduced long-term depression in the hippocampal dentate gyrus.

Citing Articles

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