Literature DB >> 24753016

Asymmetrical expression of BDNF and NTRK3 genes in frontoparietal cortex of stress-resilient rats in an animal model of depression.

Sara Farhang1, Jaleh Barar, Ali Fakhari, Mehran Mesgariabbasi, Sajjad Khani, Yadollah Omidi, Alireza Farnam.   

Abstract

The current study is based on the "approach-withdrawal" theory of emotional regulation and lateralization of brain function in rodents, which has little been studied. The aim was to indentify asymmetry in hemispheric genes expression during depression. Depressive-like symptoms were induced in rats using chronic mild stress protocol. The sucrose consumption test was performed to identify the anhedonic and stress-resilient rats. After decapitation, RNA was extracted from frontotemporal cortex of both hemispheres of anhedonic and stress-resilient rats. The pattern of gene expression in these samples was compared with controls by real-time polymerase chain reaction. A linear mixed model analysis of variance was fitted to the data to estimate the effect of rat line. From the total of 30 rats in the experimental group, five rats were identified to be anhedonic and five were stress-resilient, according to the result of sucrose-consumption test. BDNF and NTRK-3 were expressed at significantly lower levels in the right hemisphere of anhedonic rats compared with stress-resilient rats. No significant difference was found between left hemispheres. Hemispheric asymmetry in the level of gene expression was only observed for the BDNF gene in stress-resilient rats, upregulated in right hemisphere compared with the left. Expression of NTRK3, HTR2A, COMT, and SERT was not lateralized. There was no significant asymmetry between hemispheres of anhedonic rats. This study supports the evidence for the role of genes responsible for neural plasticity in pathophysiology of depression, emphasizing probable hemispheric asymmetry at level of gene expression.
Copyright © 2014 Wiley Periodicals, Inc.

Entities:  

Keywords:  BDNF; NTRK3; chronic mild stress; depression; gene expression; lateralization

Mesh:

Substances:

Year:  2014        PMID: 24753016     DOI: 10.1002/syn.21746

Source DB:  PubMed          Journal:  Synapse        ISSN: 0887-4476            Impact factor:   2.562


  11 in total

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