Document Detail


Restoration of neuroendocrine stress response by glucocorticoid receptor or GABA(A) receptor antagonists after experimental traumatic brain injury.
MedLine Citation:
PMID:  23384619     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We previously reported that traumatic brain injury (TBI) produced by moderate controlled cortical impact (CCI) attenuates the stress response of the hypothalamic-pituitary-adrenal (HPA) axis between 21 and 70 days postinjury and enhances the sensitivity of the stress response to glucocorticoid negative feedback. In the current study, we investigated two possible mechanisms for the CCI-induced attenuation of the HPA stress response-i.e, glucocorticoid receptor (GR) and GABA-mediated inhibition of the HPA axis, with the GR antagonist, mifepristone (RU486), or the GABA(A)-receptor antagonist, bicuculline. In addition, we examined the effect of moderate CCI on GR and inhibitory neurons histologically in subfields of the hippocampus, medial prefrontal cortex, and amygdala. We show that at 30-min after onset of restraint stress, GR as well as GABA antagonism with MIFE or BIC, respectively, reversed the attenuating effects of moderate CCI on the stress-induced HPA response. Our histological results demonstrate that moderate CCI led to a loss of glutamic acid decarboxylase 67 or parvalbumin-positive inhibitory neurons within regions of the hippocampus and amygdala but did not lead to significant increases in GR in these regions. These findings indicate that suppression of the stress-induced HPA response after moderate CCI is mediated by the inhibitory actions of both GR and GABA, with a corresponding loss of inhibitory neurons within brain regions with neural pathways affecting limbic stress-integrative pathways.
Authors:
Anna N Taylor; Delia L Tio; Richard L Sutton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-06-27
Journal Detail:
Title:  Journal of neurotrauma     Volume:  30     ISSN:  1557-9042     ISO Abbreviation:  J. Neurotrauma     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-07-16     Completed Date:  2014-02-12     Revised Date:  2014-08-04    
Medline Journal Info:
Nlm Unique ID:  8811626     Medline TA:  J Neurotrauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1250-6     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Amygdala / drug effects,  pathology
Analysis of Variance
Animals
Bicuculline / pharmacology
Body Weight / drug effects
Brain Injuries / drug therapy*,  physiopathology
Cell Count
Corticosterone / blood
Functional Laterality / physiology
GABA-A Receptor Antagonists / pharmacology*
Glutamate Decarboxylase / metabolism
Hippocampus / drug effects,  pathology
Hypothalamo-Hypophyseal System / drug effects
Image Processing, Computer-Assisted
Immunohistochemistry
Male
Mifepristone / pharmacology
Neurosecretory Systems / physiopathology*
Parvalbumins / metabolism
Prefrontal Cortex / drug effects,  pathology
Rats
Rats, Sprague-Dawley
Receptors, Glucocorticoid / drug effects*,  metabolism
Stress, Physiological / drug effects*
Chemical
Reg. No./Substance:
0/GABA-A Receptor Antagonists; 0/Parvalbumins; 0/Receptors, Glucocorticoid; 320T6RNW1F/Mifepristone; EC 4.1.1.15/Glutamate Decarboxylase; EC 4.1.1.15/glutamate decarboxylase 1; W980KJ009P/Corticosterone; Y37615DVKC/Bicuculline
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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