title: Genotype-dependent consequences of traumatic stress in four inbred mouse strains.
abstract: Post-traumatic stress disorder (PTSD) is an anxiety disorder that develops in predisposed individuals following a terrifying event. Studies on isogenic animal populations might explain susceptibility to PTSD by revealing associations between the molecular and behavioural consequences of traumatic stress. Our study employed four inbred mouse strains to search for differences in post-stress response to a 1.5-mA electric foot shock. One day to 6 weeks after the foot shock anxiety, depression and addiction-like phenotypes were assessed. In addition, expression levels of selected stress-related genes were analysed in hippocampus and amygdala. C57BL/6J mice exhibited up-regulation in the expression of Tsc22d3, Nfkbia, Plat and Crhr1 genes in both brain regions. These alterations were associated with an increase of sensitized fear and depressive-like behaviour over time. Traumatic stress induced expression of Tsc22d3, Nfkbia, Plat and Fkbp5 genes and developed social withdrawal in DBA/2J mice. In 129P3/J strain, exposure to stress produced the up-regulation of Tsc22d3 and Nfkbia genes and enhanced sensitivity to the rewarding properties of morphine. Whereas, SWR/J mice displayed increase only in Pdyn expression in the amygdala and had the lowest conditioned fear. Our results reveal a complex genetic background of phenotypic variation in response to stress and indicate the SWR/J strain as a valuable model of stress resistance. We found potential links between the alterations in expression of Tsc22d3, Nfkbia and Pdyn, and different aspects of susceptibility to stress.
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland.
authors.forename: K
authors.initials: K
authors.lastname: Szklarczyk
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Korostynski
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland.
authors.forename: S
authors.initials: S
authors.lastname: Golda
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland.
authors.forename: W
authors.initials: W
authors.lastname: Solecki
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland.
authors.forename: R
authors.initials: R
authors.lastname: Przewlocki
mesh_terms: D000679:Amygdala / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D004597:Electroshock; D004745:Enkephalins / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006624:Hippocampus / Q000378:metabolism; D020672:I-kappa B Proteins; D051379:Mice; D008815:Mice, Inbred Strains; D000072000:NF-KappaB Inhibitor alpha; D010641:Phenotype; D011498:Protein Precursors / Q000235:genetics; D013045:Species Specificity; D013313:Stress Disorders, Post-Traumatic / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics
chemical_list: C498608:Dsip1 protein, mouse; D004745:Enkephalins; D020672:I-kappa B Proteins; C000606205:Nfkbia protein, mouse; D011498:Protein Precursors; D014157:Transcription Factors; D000072000:NF-KappaB Inhibitor alpha; C033660:preproenkephalin