|Restoration of neuroendocrine stress response by glucocorticoid receptor or GABA(A) receptor antagonists after experimental traumatic brain injury.|
|PMID: 23384619 Owner: NLM Status: MEDLINE|
|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.|
|Anna N Taylor; Delia L Tio; Richard L Sutton|
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|Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2013-06-27|
|Title: Journal of neurotrauma Volume: 30 ISSN: 1557-9042 ISO Abbreviation: J. Neurotrauma Publication Date: 2013 Jul|
|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|
|Languages: eng Pagination: 1250-6 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Analysis of Variance
Bicuculline / pharmacology
Body Weight / drug effects
Brain Injuries / drug therapy*, physiopathology
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
Mifepristone / pharmacology
Neurosecretory Systems / physiopathology*
Parvalbumins / metabolism
Prefrontal Cortex / drug effects, pathology
Receptors, Glucocorticoid / drug effects*, metabolism
Stress, Physiological / drug effects*
|0/GABA-A Receptor Antagonists; 0/Parvalbumins; 0/Receptors, Glucocorticoid; 320T6RNW1F/Mifepristone; EC 220.127.116.11/Glutamate Decarboxylase; EC 18.104.22.168/glutamate decarboxylase 1; W980KJ009P/Corticosterone; Y37615DVKC/Bicuculline|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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