Citation

Zhang BL, Fan YS, Wang JW, Zhou ZW, Wu YG, Yang MC, Sun DD, Zhang JN. Neural Regen. Res. 2018; 13(10): 1753-1758.

Affiliation

Department of Neurosurgery, Tianjin Medical University General Hospital; Tianjin Neurological Institute; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education; Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China.

Copyright

(Copyright © 2018, Neural Regeneration Research, Shenyang, Liaoning Province, P.R. China, Publisher Wolters Kluwer)

DOI

10.4103/1673-5374.238618

PMID

30136690

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.

Language: en

Keywords

cholecystokinin; dentate gyrus; electrophysiology; excitability; hippocampus; interneurons; long-term depression; nerve regeneration; neural regeneration; parvalbumin; quantification; traumatic brain injury