Journal of Environmental Biology

Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury

Paper received:? 11.01.2019??????????????????????????????????????????????????????????? Revised received:? 25.03.2019???????????????????????????????????????????????????????????? Accepted: 30.04.2019

Authors Info

Y.H. Yu, J.H. Kang, K.H. Lee,

D.Y. Yoo, D.K. Park and

D.S. Kim*     

Department of Anatomy, Soonchunhyang University, Cheonan, 31151, Republic of Korea

*Corresponding Author Email :

dskim@sch.ac.kr

Abstract

Aim: The aim of this study was to determine whether alteration of interneurons in the hippocampus might play a role in neuronal damage caused by brain trauma and whether immunohisto chemical expressions in the hippocampus might change during the adaptive stage as early time point following traumatic brain injury (TBI).    

Methodology: For the study, we used Sprague-Dawley (SD) rats and manufactured TBI animal model by creating cryogenic injury to specific brain tissue. Thereafter, immunohisto chemical approaches were utilized to determine parvalbumin (PV) and calbindin D-28K (CB) expression in the hippocampus following brain trauma in a time course. All hippocampal tissues were analyzed qualitatively and quantitatively using immunoreactivity, cell counting and densitometry. Statistical significance was determined by one-way ANOVA and Bonferroni's test.    

Results: At early time period following TBI, both PVand CB immunoreactivities decreased in the lesioned hippocampus. However, their expression levels were recovered to control levels as time passed by. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced whereas CB expression remained unchanged.    

Interpretation: Results of this study revealed that altered distribution of interneuronal populations in the hippocampus might contribute to neuronal loss induced by abnormality of inhibitory neurotransmission at early time period following brain damage, thus leading to the development of epileptogenesis in patients with TBI.

Key words: Calbindin D-28K, Epileptogenesis, Parvalbumin, Post-traumatic epilepsy, Traumatic brain injury

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