scholarly journals Contrasting characteristic behaviours among common laboratory mouse strains

2019 ◽  
Vol 6 (6) ◽  
pp. 190574 ◽  
Author(s):  
Razia Sultana ◽  
Olalekan M. Ogundele ◽  
Charles C. Lee

Mice are widely used to model wide-ranging human neurological disorders, from development to degenerative pathophysiology. Behavioural and molecular characteristics of these mouse models are influenced by the genetic background of each strain. Among the most commonly used strains, the inbred C57BL/6J, BALB/c, CBA and 129SvEv lines and the CD1 outbred line are particularly predominant. Despite their prevalence, comparative performance of these strains on many standard behavioural tests commonly used to assess neurological conditions remains diffusely and indirectly accessible in the literature. Given that independent studies may be conducted with mice of differing genetic backgrounds, any variation in characteristic behavioural responses of specific strains should be delineated in order to properly interpret results among studies. Thus, in the present study, we aimed to characterize these commonly used mice strains through several standard behavioural tests. Here, we found that animals from different genetic background strains exhibited varying behavioural patterns when assessed for sociability/novelty, memory function, and negative behaviours like despair and stress calls. These results suggest that genetic variation among strains may be responsible—in part—for strain-specific behavioural phenotypes and potential predisposition to some neurological disorders.

2020 ◽  
Vol 115 (6) ◽  
Author(s):  
Rebekka Medert ◽  
Andy Pironet ◽  
Lucas Bacmeister ◽  
Sebastian Segin ◽  
Juan E. Camacho Londoño ◽  
...  

AbstractTransient receptor potential melastatin 4 (TRPM4) cation channels act in cardiomyocytes as a negative modulator of the L-type Ca2+ current. Ubiquitous Trpm4 deletion in mice leads to an increased β-adrenergic inotropy in healthy mice as well as after myocardial infarction. In this study, we set out to investigate cardiac inotropy in mice with cardiomyocyte-specific Trpm4 deletion. The results guided us to investigate the relevance of TRPM4 for catecholamine-evoked Ca2+ signaling in cardiomyocytes and inotropy in vivo in TRPM4-deficient mouse models of different genetic background. Cardiac hemodynamics were investigated using pressure–volume analysis. Surprisingly, an increased β-adrenergic inotropy was observed in global TRPM4-deficient mice on a 129SvJ genetic background, but the inotropic response was unaltered in mice with global and cardiomyocyte-specific TRPM4 deletion on the C57Bl/6N background. We found that the expression of TRPM4 proteins is about 78 ± 10% higher in wild-type mice on the 129SvJ versus C57Bl/6N background. In accordance with contractility measurements, our analysis of the intracellular Ca2+ transients revealed an increase in ISO-evoked Ca2+ rise in Trpm4-deficient cardiomyocytes of the 129SvJ strain, but not of the C57Bl/6N strain. No significant differences were observed between the two mouse strains in the expression of other regulators of cardiomyocyte Ca2+ homeostasis. We conclude that the relevance of TRPM4 for cardiac contractility depends on homeostatic TRPM4 expression levels or the genetic endowment in different mouse strains as well as on the health/disease status. Therefore, the concept of inhibiting TRPM4 channels to improve cardiac contractility needs to be carefully explored in specific strains and species and prospectively in different genetically diverse populations of patients.


2011 ◽  
Vol 11 ◽  
pp. 429-436 ◽  
Author(s):  
Eli Reuveni

Laboratory mouse strains are known for their large phenotypic diversity and serve as a primary mammalian model in genotype-phenotype association studies. One possible attempt to understand the reason for this diversity could be addressed by careful investigation of the unique evolutionary history of their wild-derived founders and the consequence that it may have on the genetic makeup of the laboratory mouse strains during the history of human fancy breeding. This review will summarize recently published literature that endeavors to unravel the genetic background of laboratory mouse strains, as well as give new insights into novel evolutionary approaches. I will explain basic concepts of molecular evolution and the reason why it is important in order to infer function even among closely related wild and domesticated species. I will also discuss future frontiers in the field and how newly emerging sequencing technologies could help us to better understand the relationship between genotype and phenotype.


Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 342
Author(s):  
In Sook Ahn ◽  
Justin Yoon ◽  
Graciel Diamante ◽  
Peter Cohn ◽  
Cholsoon Jang ◽  
...  

High fructose consumption has been linked to metabolic syndrome, yet the fructose-induced phenotypes, gene expression, and gut microbiota alterations are distinct between mouse strains. In this study, we aim to investigate how fructose consumption shapes the metabolomic profiles of mice with different genetic background and microbiome. We used fructose-sensitive DBA/2J (DBA) and fructose-resistant C57BL/6J (B6) mice given 8% fructose or regular water for 12 weeks. Plasma and fecal metabolites were profiled using a liquid chromatography-tandem mass spectrometry based global metabolomic approach. We found that the baseline metabolomic profiles were different between DBA and B6 mice, particularly plasma metabolites involved in lipid metabolism and fecal metabolites related to dipeptide/amino acid metabolism. In response to fructose, DBA mice showed a distinct decrease of plasma branched chain fatty acids with concordantly increased branched chain amino acids, which were correlated with adiposity; B6 mice had significantly increased plasma cholesterol and total bile acids, accompanied by decreased fecal levels of farnesoid X receptor antagonist tauro-β-muricholate, which were correlated with fructose-responsive bacteria Dehalobacterium, Magibacteriaceae, and/or Akkermansia. Our results demonstrate that baseline metabolomic profiles differ and respond differentially to fructose between mice with different genetic background and gut microbiota, which may play a role in individualized risks to fructose-induced metabolic syndrome.


2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Manan Binth Taj Noor ◽  
Nusrat Zerin Zenia ◽  
M Shamim Kaiser ◽  
Shamim Al Mamun ◽  
Mufti Mahmud

Abstract Neuroimaging, in particular magnetic resonance imaging (MRI), has been playing an important role in understanding brain functionalities and its disorders during the last couple of decades. These cutting-edge MRI scans, supported by high-performance computational tools and novel ML techniques, have opened up possibilities to unprecedentedly identify neurological disorders. However, similarities in disease phenotypes make it very difficult to detect such disorders accurately from the acquired neuroimaging data. This article critically examines and compares performances of the existing deep learning (DL)-based methods to detect neurological disorders—focusing on Alzheimer’s disease, Parkinson’s disease and schizophrenia—from MRI data acquired using different modalities including functional and structural MRI. The comparative performance analysis of various DL architectures across different disorders and imaging modalities suggests that the Convolutional Neural Network outperforms other methods in detecting neurological disorders. Towards the end, a number of current research challenges are indicated and some possible future research directions are provided.


2015 ◽  
Vol 11 (7) ◽  
pp. 781-793 ◽  
Author(s):  
Lei Sheng ◽  
Wenbo Chai ◽  
Xuefeng Gong ◽  
Lingyan Zhou ◽  
Ronghao Cai ◽  
...  

2002 ◽  
Vol 9 (3) ◽  
pp. 151-159 ◽  
Author(s):  
Geert Raes ◽  
Wim Noël ◽  
Alain Beschin ◽  
Lea Brys ◽  
Patrick de Baetselier ◽  
...  

Although it is well-established that macrophages can occur in distinct activation states, the molecular characteristics of differentially activated macrophages, and particularly those of alternatively activated macrophages (aaMφ), are still poorly unraveled. Recently, we demonstrated that the expression of FIZZ1 and Ym is induced in aaMφ as compared with classically activated macrophages (caMφ), elicitedin vitroor developedin vivoduring infection withTrypanosoma brucei brucei. In the present study, we analyzed the expression of FIZZ1 and Ym in caMφ and aaMφ elicited duringTrypanosoma congolenseinfection and show that the use of FIZZ1 and Ym for the identification of aaMφ is not limited toT. b. bruceiinfection and is independent of the organ sources from which macrophages are obtained. We also demonstrate that FIZZ1 can be used to discriminate between different populations of aaMφ. Furthermore, we studied the effects of various stimuli, and combinations thereof, on the expression of FIZZ1 and Ym in macrophages from different mouse strains and demonstrate that regulation of the expression of FIZZ1 and Ym in macrophages is not dependent on the mouse strain. Finally, we show that these genes can be used to monitor the macrophage activation status without the need to obtain pure macrophage populations.


1997 ◽  
Vol 3 (S2) ◽  
pp. 317-318
Author(s):  
David A. Sanan ◽  
Dale L. Newland

Build-up of visible atherosclerotic plaque in the arteries is readily quantifiable. The mouse and the rabbit provide useful models for understanding the pathogenesis of atherosclerosis by investigating the effects of genetic and dietary perturbations.Although the wild type mouse does not develop atherosclerosis, atherosclerosis susceptibility genes have been identified in some laboratory mouse strains which do. Furthermore, transgenic technology and gene targeting have produced genetically modified mice that express various apolipoproteins, enzymes and cofactors involved in human lipoprotein metabolism. Gene “knockout” technology allows transgene expression without interference from homologous genes. One notable “knockout” mouse, deficient in apolipoprotein E, develops spontaneous atherosclerosis on a normal chow diet. Transgenic modulations of the atherosclerotic responses of these highly susceptible mice are more pronounced and easily measured. Small, cheap and fast breeding, mice are convenient animal models. But to make mice susceptible to atherosclerosis, their genetic background has to be so drastically altered that the resulting lipoprotein metabolism may not model the human metabolism accurately enough.


Cryobiology ◽  
2010 ◽  
Vol 60 (2) ◽  
pp. 129-137 ◽  
Author(s):  
Kuo-Yu Huang ◽  
Suzanna A. de Groot ◽  
Henri Woelders ◽  
Gijsbertus T.J. van der Horst ◽  
Axel P.N. Themmen ◽  
...  

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