scholarly journals Impaired Pavlovian fear extinction is a common phenotype across genetic lineages of the 129 inbred mouse strain

2009 ◽  
Vol 8 (8) ◽  
pp. 744-752 ◽  
Author(s):  
M. Camp ◽  
M. Norcross ◽  
N. Whittle ◽  
M. Feyder ◽  
W. D’Hanis ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eva Maria Fritz ◽  
Matthias Kreuzer ◽  
Alp Altunkaya ◽  
Nicolas Singewald ◽  
Thomas Fenzl

AbstractSleep disturbances are a common complaint of anxiety patients and constitute a hallmark feature of post-traumatic stress disorder (PTSD). Emerging evidence suggests that poor sleep is not only a secondary symptom of anxiety- and trauma-related disorders but represents a risk factor in their development, for example by interfering with emotional memory processing. Fear extinction is a critical mechanism for the attenuation of fearful and traumatic memories and multiple studies suggest that healthy sleep is crucial for the formation of extinction memories. However, fear extinction is often impaired in anxiety- and trauma-related disorders—an endophenotype that is perfectly modelled in the 129S1/SvImJ inbred mouse strain. To investigate whether these mice exhibit altered sleep at baseline that could predispose them towards maladaptive fear processing, we compared their circadian sleep/wake patterns to those of typically extinction-competent C57BL/6 mice. We found significant differences regarding diurnal distribution of sleep and wakefulness, but also sleep architecture, spectral features and sleep spindle events. With regard to sleep disturbances reported by anxiety- and PTSD patients, our findings strengthen the 129S1/SvImJ mouse models’ face validity and highlight it as a platform to investigate novel, sleep-focused diagnostic and therapeutic strategies. Whether the identified alterations causally contribute to its pathological anxiety/PTSD-like phenotype will, however, have to be addressed in future studies.


2010 ◽  
Vol 78 (9) ◽  
pp. 3848-3860 ◽  
Author(s):  
Lien Dejager ◽  
Iris Pinheiro ◽  
Pieter Bogaert ◽  
Liesbeth Huys ◽  
Claude Libert

ABSTRACT Infection with Salmonella enterica serovar Typhimurium is a complex disease in which the host-bacterium interactions are strongly influenced by genetic factors of the host. We demonstrate that SPRET/Ei, an inbred mouse strain derived from Mus spretus, is resistant to S. Typhimurium infections. The kinetics of bacterial proliferation, as well as histological examinations of tissue sections, suggest that SPRET/Ei mice can control bacterial multiplication and spreading despite significant attenuation of the cytokine response. The resistance of SPRET/Ei mice to S. Typhimurium infection is associated with increased leukocyte counts in the circulation and enhanced neutrophil influx into the peritoneum during the course of infection. A critical role of neutrophils was confirmed by neutrophil depletion: neutropenic SPRET/Ei mice were sensitive to infection with S. Typhimurium and showed much higher bacterial loads. To identify genes that modulate the natural resistance of SPRET/Ei mice to S. Typhimurium infection, we performed a genome-wide study using an interspecific backcross between C3H/HeN and SPRET/Ei mice. The results of this analysis demonstrate that at least two loci, located on chromosomes 6 and 11, affect survival following lethal infection with S. Typhimurium. These two loci contain several interesting candidate genes which may have important implications for the search for genetic factors controlling Salmonella infections in humans and for our understanding of complex host-pathogen interactions in general.


2018 ◽  
Vol 29 (7-8) ◽  
pp. 585-592
Author(s):  
Steven Timmermans ◽  
Jolien Souffriau ◽  
Jolien Vandewalle ◽  
Lise Van Wyngene ◽  
Kelly Van Looveren ◽  
...  

1985 ◽  
Vol 46 (3) ◽  
pp. 349-352 ◽  
Author(s):  
John D. West ◽  
Mary F. Lyon ◽  
Josephine Peters ◽  
Paul B. Selby

SUMMARYGenetic polymorphisms revealed two distinct substrains of the inbred strain 101. One group included substrains 101*/Rl, 101/H and 101/HOxe; the other group comprised 101/El and 101/Sl. The two groups differed at 5 of the 8 genetic loci tested. The accompanying paper (Evans, Burtenshaw & Adler, 1985) shows that the two groups also differ for several chromosome polymorphisms. We suggest that genetic contamination occurred during the derivation of 101/El from 101/Rl and was already present in 101/El when 101/Sl was produced from this substrain. We further propose that these substrains be renamed 102/El and 102/Sl respectively.


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