Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression

Autor: Jennifer L. McGuire, Maxon V. Knott, Judy Bohnert, Erika A. Correll, Laura B. Ngwenya, Noah J. Ziemba, Emily Allgire, Tracy Hopkins
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
medicine.medical_specialty
QH301-705.5
Traumatic brain injury
hippocampus
glutamate receptor
Wistar Kyoto
Hippocampus
Hippocampal formation
Rats
Inbred WKY
Receptors
N-Methyl-D-Aspartate
Catalysis
Article
Inorganic Chemistry
03 medical and health sciences
Myelin
Glutamatergic
0302 clinical medicine
Internal medicine
Brain Injuries
Traumatic
medicine
Animals
Biology (General)
Physical and Theoretical Chemistry
Rats
Wistar
QD1-999
Molecular Biology
Spectroscopy
Depression (differential diagnoses)
Cell Proliferation
Depressive Disorder
Major
business.industry
Dentate gyrus
traumatic brain injury
Organic Chemistry
Glutamate receptor
General Medicine
medicine.disease
Computer Science Applications
Rats
Chemistry
030104 developmental biology
Endocrinology
medicine.anatomical_structure
depression
sense organs
business
030217 neurology & neurosurgery
Zdroj: International Journal of Molecular Sciences
Volume 22
Issue 15
International Journal of Molecular Sciences, Vol 22, Iss 8086, p 8086 (2021)
ISSN: 1422-0067
Popis: Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many commonalities including volume changes, myelin disruption, changes in proliferation, and changes in glutamatergic signaling. We used a well-established animal model of depression, the Wistar Kyoto (WKY) rat, to elucidate changes after TBI that may influence the recovery trajectory. We compared the histological and molecular outcomes in the hippocampal dentate gyrus after experimental TBI using the lateral fluid percussion injury (LFPI) in the WKY and the parent Wistar (WIS) strain. We showed that WKY had exaggerated myelin loss after LFPI and baseline deficits in proliferation. In addition, we showed that while after LFPI WIS rats exhibited glutamate receptor subunit changes, namely increased GluN2B, the WKY rats failed to show such injury-related changes. These differential responses to LFPI helped to elucidate the molecular characteristics that influence poor recovery after TBI in those with pre-existing depression and may lead to targets for future therapeutic interventions.
Databáze: OpenAIRE
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