Document Detail


TBI and sex: crucial role of progesterone protecting the brain in an omega-3 deficient condition.
MedLine Citation:
PMID:  24361060     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We assessed whether the protective action of progesterone on traumatic brain injury (TBI) could be influenced by the consumption of omega-3 fatty acids during early life. Pregnant Sprague-Dawley rats were fed on omega-3 adequate or deficient diet from 3rd day of pregnancy and their female offspring were kept on the same diets up to the age of 15 weeks. Ovariectomy was performed at the age of 12 weeks to deprive animals from endogenous steroids until the time of a fluid percussion injury (FPI). Dietary n-3 fatty acid deficiency increased anxiety in sham animals and TBI aggravated the effects of the deficiency. Progesterone replacement counteracted the effects of TBI on the animals reared under n-3 deficiency. A similar pattern was observed for markers of membrane homeostasis such as 4-Hydroxynonenal (HNE) and secreted phospholipases A2 (sPLA2), synaptic plasticity such as brain derived neurotrophic factor (BDNF), syntaxin (STX)-3 and growth associated protein (GAP)-43, and for growth inhibitory molecules such as myelin-associated glycoprotein (MAG) and Nogo-A. Results that progesterone had no effects on sham n-3 deficient animals suggest that the availability of progesterone is essential under injury conditions. Progesterone treatment counteracted several parameters related to synaptic plasticity and membrane stability reduced by FPI and n-3 deficiency suggest potential targets for therapeutic applications. These results reveal the importance of n-3 preconditioning during early life and the efficacy of progesterone therapy during adulthood to counteract weaknesses in neuronal and behavioral plasticity.
Authors:
Ethika Tyagi; Rahul Agrawal; Zhe Ying; Fernando Gomez-Pinilla
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-12-18
Journal Detail:
Title:  Experimental neurology     Volume:  253     ISSN:  1090-2430     ISO Abbreviation:  Exp. Neurol.     Publication Date:  2014 Mar 
Date Detail:
Created Date:  2014-02-19     Completed Date:  2014-04-07     Revised Date:  2014-05-07    
Medline Journal Info:
Nlm Unique ID:  0370712     Medline TA:  Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  41-51     Citation Subset:  IM    
Copyright Information:
Copyright © 2014 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Anxiety / drug therapy,  etiology
Brain Injuries / complications,  etiology,  prevention & control*
Dietary Fats / pharmacology*
Disease Models, Animal
Fatty Acids / metabolism
Fatty Acids, Omega-3 / metabolism,  pharmacology*
Female
GAP-43 Protein / metabolism
Male
Maze Learning / drug effects
Myelin Proteins / toxicity
Myelin-Associated Glycoprotein / toxicity
Neuropeptide Y / metabolism
Ovariectomy
Pregnancy
Prenatal Exposure Delayed Effects
Progesterone / therapeutic use*
Progestins / therapeutic use*
Qa-SNARE Proteins / metabolism
Rats
Rats, Sprague-Dawley
Sex Factors
Grant Support
ID/Acronym/Agency:
NS050465/NS/NINDS NIH HHS; NS056413/NS/NINDS NIH HHS; R01 NS050465/NS/NINDS NIH HHS; R01 NS056413/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Fatty Acids; 0/Fatty Acids, Omega-3; 0/GAP-43 Protein; 0/Myelin Proteins; 0/Myelin-Associated Glycoprotein; 0/Neuropeptide Y; 0/Nogo protein; 0/Progestins; 0/Qa-SNARE Proteins; 4G7DS2Q64Y/Progesterone

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


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