Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury

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...

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Bibliographic Details
Published in:Journal of environmental biology 2019-09, Vol.40 (5(SI)), p.833-840
Main Authors: Yu, Y.H., Kang, J.H., Lee, K.H., Yoo, D.Y., Park, D.K., Kim, D.S.
Format: Article
Language:English
Subjects:
Animal models
Brain
Brain damage
Calbindin-D28K
Convulsions & seizures
Densitometers
Densitometry
Epilepsy
Head injuries
Hippocampus
Immunoreactivity
Interneurons
Laboratory animals
Medical prognosis
Neurotransmission
Organic chemistry
Parvalbumin
Pathogenesis
Rodents
Trauma
Traumatic brain injury
Variance analysis
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Summary: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.
ISSN:0254-8704
2394-0379
DOI:10.22438/jeb/40/5(SI)/SI-02