Journal articles: 'Inbred rat'

1

Thomas, Michael A., Chin-Fu Chen, Michael I. Jensen-Seaman, Peter J. Tonellato, and Simon N. Twigger. "Phylogenetics of rat inbred strains." Mammalian Genome 14, no. 1 (January 1, 2003): 61–64. http://dx.doi.org/10.1007/s00335-002-2204-5.

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Kuramoto, Takashi, Satoshi Nakanishi, and Tadao Serikawa. "Functional polymorphisms in inbred rat strains and their allele frequencies in commercially available outbred stocks." Physiological Genomics 33, no. 2 (April 2008): 205–11. http://dx.doi.org/10.1152/physiolgenomics.00222.2007.

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Polymorphisms that have been proven to influence gene functions are called functional polymorphisms. It is significant to know the distribution of functional polymorphisms in the rat, widely used in animal models for human diseases. In this study, we assessed 16 functional polymorphisms consisting of 3 coat color and 13 disease-associated genes in 136 rat strains, as a part of the genetic profiling program of the National Bio Resource Project for the Rat (NBRP-Rat). Polymorphisms of Cdkn1a, Fcgr3, Grp10, Lss, and Fdft1, which were proven to function in prostate tumorigenesis, glomerulonephritis, hyperphagia, and cholesterol biosynthesis, were shared among various inbred strains. These findings indicated that most rat strains harbored the disease-associated alleles and suggested that many unidentified functional polymorphisms might exist in inbred rat strains. The functional polymorphisms shared in inbred strains were also observed within outbred stocks available commercially. Therefore, this implies that experimental plans based on either rat inbred strains or outbred stocks need to be carefully designed with a full understanding of the genetic characteristics of the animals. To select the most suitable strains for experiments, the NBRP-Rat will periodically improve and update the genetic profiles of rat strains.

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Kren, V., T. W. Kurtz, D. Krenova, V. Bila, M. Printz, and P. Pravenec. "Rat genome mapping using recombinant inbred strains." Transplantation Proceedings 29, no. 3 (May 1997): 1768. http://dx.doi.org/10.1016/s0041-1345(97)00048-1.

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Schlick, Nancy E., Michael I. Jensen-Seaman, Kimberly Orlebeke, Anne E. Kwitek, Howard J. Jacob, and Jozef Lazar. "Sequence analysis of the complete mitochondrial DNA in 10 commonly used inbred rat strains." American Journal of Physiology-Cell Physiology 291, no. 6 (December 2006): C1183—C1192. http://dx.doi.org/10.1152/ajpcell.00234.2006.

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Rat remains a major biomedical model system for common, complex diseases. The rat continues to gain importance as a model system with the completion of its full genomic sequence. Although the genomic sequence has generated much interest, only three complete sequences of the rat mitochondria exist. Therefore, to increase the knowledge of the rat genome, the entire mitochondrial genomes (16,307–16,315 bp) from 10 inbred rat strains (that are standard laboratory models around the world) and 2 wild rat strains were sequenced. We observed a total of 195 polymorphisms, 32 of which created an amino acid change (nonsynonymous substitutions) in 12 of the 13 protein coding genes within the mitochondrial genome. There were 11 single nucleotide polymorphisms within the tRNA genes, six in the 12S rRNA, and 12 in the 16S rRNA including 3 insertions/deletions. We found 14 single nucleotide polymorphisms and 2 insertion/deletion polymorphisms in the D-loop. The inbred rat strains cluster phylogenetically into three distinct groups. The wild rat from Tokyo grouped closely with five inbred strains in the phylogeny, whereas the wild rat from Milwaukee was not closely related to any inbred strain. These data will enable investigators to rapidly assess the potential impact of the mitochondria in these rats on the physiology and the pathophysiology of phenotypes studied in these strains. Moreover, these data provide information that may be useful as new animal models, which result in novel combinations of nuclear and mitochondrial genomes, are developed.

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Pohlová, Irena, Josef Zicha, Vladimir Křen, Jaroslav Kuneš, and Michal Pravenec. "Renal renin activity is associated with alterations of the renin gene in recombinant inbred rat strains." Clinical Science 84, no. 2 (February 1, 1993): 129–32. http://dx.doi.org/10.1042/cs0840129.

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1. A structural alteration within the first intron of the renin gene in spontaneously hypertensive rats was demonstrated to co-segregate with blood pressure in some sets of F2 hybrids or recombinant inbred strains. There is no evidence as to whether restriction fragment length polymorphism of the renin gene is associated with any of the changes in the renin tissue level. For this reason we have determined renal renin activity in spontaneously hypertensive, Wistar-Kyoto and Brown Norway rats as well as in 22 recombinant inbred strains derived from F2 hybrids of spontaneously hypertensive and Brown Norway rats. 2. At the age of 4 months significantly lower renal renin activity was observed in spontaneously hypertensive rats than in both normotensive rat strains, Wistar-Kyoto and Brown Norway. The presence of the spontaneously hypertensive rat allele in recombinant inbred strains was associated with a substantially lower renal renin activity as compared with recombinant inbred strains bearing the Brown Norway rat allele. There was no relationship between renal renin activity and the polymorphism in either the angiotensinogen gene or the angiotensin-converting enzyme gene. 3. There was a borderline correlation between blood pressure and renal renin activity in recombinant inbred strains. Nevertheless, additional comparisons within recombinant inbred strains bearing the spontaneously hypertensive rat allele of the renin gene failed to reveal any significant relationship between blood pressure level and renal renin activity. 4. Our data suggest that the restriction fragment length polymorphism marking the renin gene of the spontaneously hypertensive rat is accompanied by an alteration in the renin-angiotensin system at the renal level. The mechanisms by which structural abnormalities of the renin gene might influence the renin level in the kidney remain to be investigated.

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Bell, R. G. "Variation in responsiveness toTrichinella spiralisinfection in inbred rat strains." Parasitology 105, no. 1 (August 1992): 125–30. http://dx.doi.org/10.1017/s0031182000073777.

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An analysis of interstrain variation between 12 inbred and 4 congenic rat strains in the expression of immunity againstTrichinella spiralisis reported. All rat strains expressed strong rapid expulsion which resulted in the elimination of 88–98% of a challenge infection of muscle larvae. In contrast, substantial interstrain variation in the rate of adult worm expulsion in the primary infection as evident. By day 10 after infection, BUF and YO strains had < 50 worms left in the intestine whereas BI and WKA strain rats had barely begun rejection, with approximately 1000 worms present in the gut for both strains. All other rat strains fell within these extremes in a continuous gradation. There was no clustering of rat strains into phenotypic groups with comparable worm burdens as seen with mice. The number of muscle larvae that established after the primary infection showed less variation than had adult worm burden in the primary infection and there was only a weak correlation of muscle larvae burden with numbers of intestinal adults present at 10 days. Comparison of MHC matched or MHC-disparate rat strains on a PVG background suggested that non-MHC genes determined the principal adult worm rejection characteristics of a given strain. The absence of phenotypic variation in the expression of rapid expulsion in rats reinforces the biological distinction between rat rapid expulsion and the ‘rapid expulsion’ defined for mice

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Woo, Lynn L., Adonis Hijaz, Hui Q. Pan, Mei Kuang, Raymond R. Rackley, and Margot S. Damaser. "Simulated childbirth injuries in an inbred rat strain." Neurourology and Urodynamics 28, no. 4 (April 2009): 356–61. http://dx.doi.org/10.1002/nau.20644.

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8

Sprott, R. L., and I. Ramirez. "Current Inbred and Hybrid Rat and Mouse Models." ILAR Journal 38, no. 3 (January 1, 1997): 104–9. http://dx.doi.org/10.1093/ilar.38.3.104.

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Leyten, R., J. P. A. M. Vroemen, N. Blanckaert, and K. P. M. Heirwegh. "The congenic normal R/APfd and jaundiced R/APfd-j/j rat strains: a new animal model of hereditary non-haemolytic unconjugated hyperbilirubinaemia due to defective bilirubin conjugation." Laboratory Animals 20, no. 4 (October 1, 1986): 335–42. http://dx.doi.org/10.1258/002367786780808758.

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In this paper the production of the R/APfd-j/j strain which is congenic with the R/APfd strain is reported. The R/APfd-j/j completely lacks hepatic bilirubin UDP-glucuronyltransferase activity, as do our GUNNXR/Pfd-j/j rat strain and various other stocks of GUNN rats (j/j) described in the literature. Our recombinant inbred strain GUNNXR/Pfd-j/j was produced from non-inbred GUNN (j/j) rats. This GUNNXR/Pfd-j/j rat was used as a donor of the jaundice gene j, the R/APfd rat serving as the recipient. After eight backcross-intercross cycles (16 generations) the R/APfd-j/j strain was obtained which is congenic with the R/APfd strain. Congenicity was demonstrated by various techniques including transplantation of skin tissue, strain-specific tumour cells and hepatocytes, the mixed lymphocyte reaction, and comparison of biochemical markers. The potential of the novel inbred strain of jaundiced rat, R/APfd-j/j, and the corresponding control strain R/APfd for biochemical and clinical studies of bilirubin metabolism are briefly discussed.

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Power, D. A., C. Cunningham, and G. R. D. Catto. "The role of RT1 antigen differences in semi-allogeneic rat pregnancy." Clinical Science 72, no. 1 (January 1, 1987): 37–45. http://dx.doi.org/10.1042/cs0720037.

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1. The immunological mechanisms involved in sustaining normal semi-allogeneic pregnancies and in the enhancement of organ allografts were investigated in inbred rats. 2. The antigenic targets for alloantibodies formed after leucocyte transfusions and multiple allogeneic pregnancies were defined by the EA rosette inhibition (EAI) assay in several congenic and recombinant inbred rat strains. 3. Alloantibodies produced by leucocyte immunization (conventionally induced antisera) were directed only to RT1-encoded (major histocompatibility complex, MHC) antigens. Both RT1A (class I MHC) and either RT1B, D (class II MHC) or RT1C (Qa-like) antigens were targets for these alloantibodies; responses to the latter three antigens could not be separated with available congenic recombinant inbred rat strains. 4. Alloantibodies produced as a consequence of multiple semi-allogeneic pregnancies (pregnancy-induced antisera) were directed only to RT1A antigens. 5. Allogeneic pregnancies in which the paternal strain differed from the maternal strain only at the RT1A gene locus produced suppression of a subsequent maternal immune response.

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11

Wang, C. G., J. J. Almirall, C. S. Dolman, R. J. Dandurand, and D. H. Eidelman. "In vitro bronchial responsiveness in two highly inbred rat strains." Journal of Applied Physiology 82, no. 5 (May 1, 1997): 1445–52. http://dx.doi.org/10.1152/jappl.1997.82.5.1445.

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Wang, C. G., J. J. Almirall, C. S. Dolman, R. J. Dandurand, and D. H. Eidelman. In vitro bronchial responsiveness in two highly inbred rat strains. J. Appl. Physiol. 82(5): 1445–1452, 1997.—We investigated methacholine (MCh)-induced bronchoconstriction in explanted airways from Fischer and Lewis rats. Lung explants, 0.5- to 1.0-mm thick, were prepared from agarose-inflated lungs of anesthetized 8- to 12-wk-old male rats. After overnight culture, videomicroscopy was used to record baseline images of the individual airways. Dose-response curves to MCh were then constructed by repeated administration of MCh; airways were reimaged 10 min after each MCh administration. Airway internal luminal area ( A i) was measured at successive MCh concentrations from 10−9 to 10−1 M. In addition to the effective concentration leading to 50% of the achieved maximal response, we also determined the effective concentration leading to a 40% reduction in A i. Both the effective concentration leading to 50% of the achieved maximal response and the concentration leading to a 40% reduction in A iwere significantly lower among Fischer rat airways ( P < 0.05). Airway closure was more common among Fischer rat airways (17%) than among those of Lewis rats (7.5%). Responsiveness of Fischer rat airways was more heterogeneous than among Lewis airways; a larger number of Fischer rat airways exhibited high sensitivity to MCh. There was no relationship between responsiveness and baseline A iin either strain. In a second experiment, we measured the rate of contraction of explanted airways from lungs inflated to 50, 75, and 100% of total lung capacity. The average rate of contraction in the first 15 s was higher in Fischer rat airways at each inflation volume. These data indicate that the hyperresponsiveness of the Fischer rat reflects the responsiveness of individual airways throughout the airway tree and are consistent with the notion that in this model hyperresponsiveness is an intrinsic property of airway smooth muscle.

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Behmoaras, Jacques, Mary Osborne-Pellegrin, Dominique Gauguier, and Marie-Paule Jacob. "Characteristics of the aortic elastic network and related phenotypes in seven inbred rat strains." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (February 2005): H769—H777. http://dx.doi.org/10.1152/ajpheart.00544.2004.

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Extracellular matrix (ECM) molecules such as elastin and collagen provide mechanical support to the vessel wall and are essential for vascular function. Evidence that genetic factors influence aortic ECM composition and organization was concluded from our previous studies showing that the inbred Brown Norway (BN) rat differs significantly from the outbred Long-Evans (LE) and the inbred LOU rat with respect to both thoracic aortic elastin content and internal elastic lamina (IEL) rupture in the abdominal aorta and iliac arteries. Here, we measured aortic elastin and collagen contents as well as factors that may modulate these parameters [insulin growth factor (IGF)-I, transforming growth factor (TGF)-β1, and matrix metalloproteinase (MMP)-2] in seven inbred rat strains, including BN and LOU. We also investigated whether IEL ruptures occur in strains other than BN. We showed that LOU, LE, BN, and Fischer 344 (F344) rats were significantly different for aortic elastin content and elastin-to-collagen ratio, whereas LE, Lewis, WAG, and Wistar-Furth (WF) were similar for these parameters. BN and F344 had the lowest values. BN was the only strain to present numerous IEL ruptures, whereas F344, LE, and WF presented a few and the other strains presented none. In addition, IGF-I and TGF-β1 levels in the plasma and aorta differed significantly between strains, suggesting genetic control of their production. Because inbred rat strains provide interesting models for quantitative trait locus analysis, our results concerning elastin, collagen, IEL ruptures, and cytokines may provide a basis for the search for candidate genes involved in the control of these phenotypes.

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KOCH, LAUREN GERARD, STEVEN L. BRITTON, JOHN C. BARBATO, DAVID W. RODENBAUGH, and STEPHEN E. DiCARLO. "Phenotypic differences in cardiovascular regulation in inbred rat models of aerobic capacity." Physiological Genomics 1, no. 2 (August 31, 1999): 63–69. http://dx.doi.org/10.1152/physiolgenomics.1999.1.2.63.

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Koch, Lauren Gerard, Steven L. Britton, John C. Barbato, David W. Rodenbaugh, and Stephen E. DiCarlo. Phenotypic differences in cardiovascular regulation in inbred rat models of aerobic capacity. Physiol. Genomics 63–69, 1999.—The Dark Aouti (DA) inbred strain of rats has superior aerobic treadmill running capacity compared with the Copenhagen (COP) strain of inbred rats. This difference in aerobic capacity provides a model to explore the genetic basis of variation in this trait. The present study evaluated intermediate phenotypic differences between 10 male COP inbred rats and 10 male DA inbred rats that might contribute to the difference in aerobic capacity between the strains. Five autonomically regulated cardiovascular variables were evaluated during rest or exercise by measuring the response to autonomic antagonists. The DA rat had enhanced autonomic function for the regulation of peripheral blood flow and cardiac output. Specifically, at rest the DA rats had significantly more sympathetic (123 ± 8 vs. 99 ± 7 beats/min) and parasympathetic (35 ± 5 vs. 12 ± 3 beats/min) tonus for heart rate control and more sympathetic support of blood pressure (70 ± 7 vs. 38 ± 6 mmHg) compared with the COP rats. During three graded levels of treadmill exercise the DA rats had higher blood pressures (16% on average) and higher heart rates (4% on average) relative to the COP rats. In addition, the DA rats had a 27% greater heart weight-to-body weight ratio compared with the COP strain of rats (3.63 ± 0.08 vs. 2.85 ± 0.07 g/kg). All five of these intermediate phenotypes could participate as variables causative of the difference in treadmill running capacity between the DA and COP strains of rats.

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Ibrahim, Jamila, Jody K. Miyashiro, and Bradford C. Berk. "Shear Stress Is Differentially Regulated Among Inbred Rat Strains." Circulation Research 92, no. 9 (May 16, 2003): 1001–9. http://dx.doi.org/10.1161/01.res.0000069687.54486.b1.

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Rosenwasser, A. M., M. W. Pellowski, and E. D. Hendley. "Circadian timekeeping in hyperactive and hypertensive inbred rat strains." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 3 (September 1, 1996): R787—R796. http://dx.doi.org/10.1152/ajpregu.1996.271.3.r787.

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Inbred strains have been used to study genetic and physiological relationships among different aspects of circadian timekeeping, as well as relationships between circadian rhythmicity and other strain-specific traits. The present study characterized several features of circadian timekeeping in genetically hyperactive (WKHA) and genetically hypertensive (WKHT) inbred strains, derived from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. WKHAs and WKHTs differed in free-running period, steady-state entrainment to light-dark cycles, and photic phase shifting, and relationships among these measures were consistent with previous studies of species, strain, and individual differences. Because both WKHTs and SHRs show short circadian periods relative to their respective comparison strains, this trait may cosegregate genetically with hypertension. In contrast, because WKHAs and SHRs show similar photic entrainment and phase shifting, these circadian functions may cosegregate with open-field hyperactivity. Finally, because neither WKHAs nor WKHTs show the SHR's excessive levels of home-cage running wheel activity, this trait is not related to either hypertension or open-field activity. Further work would be required to elucidate specific genetic and/or physiological linkages among these variables.

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ERICKSON, C., and K. BYERS. "Sustained nicotine release comparisons in six inbred rat strains." Pharmacology Biochemistry and Behavior 33, no. 1 (May 1989): 63–67. http://dx.doi.org/10.1016/0091-3057(89)90430-9.

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Zhang-James, Yanli, Li Yang, Frank A. Middleton, Lina Yang, Jameson Patak, and Stephen V. Faraone. "Autism-related behavioral phenotypes in an inbred rat substrain." Behavioural Brain Research 269 (August 2014): 103–14. http://dx.doi.org/10.1016/j.bbr.2014.04.035.

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Michalkiewicz, Mieczyslaw, Teresa Michalkiewicz, Aron M. Geurts, Richard J. Roman, Glenn R. Slocum, Oded Singer, Dorothee Weihrauch, et al. "Efficient transgenic rat production by a lentiviral vector." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H881—H894. http://dx.doi.org/10.1152/ajpheart.00060.2007.

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A lentiviral construct for an enhanced green fluorescent protein (eGFP) driven by a chicken β-actin promoter, cytomegalovirus enhancer, and intronic sequences from rabbit β-globin (CAG) was used to produce transgenic lines of rats for evaluation of the usefulness of this approach in gene function studies. Fertilized eggs were collected from inbred Dahl S and outbred Sprague-Dawley rats, and ∼100 pl of concentrated virus were microinjected into the perivitrelline space of one-cell embryos. Of 121 embryos injected, 60 pups (49.6%) were born. Transgenic rates averaged 22% in Dahl S and 14% in Sprague-Dawley rats. Copy number ranged from one to four in the founders, and the inheritance of the transgene in a subsequent F1population was 48.2%. The small number of insertion sites enabled us to derive inbred transgenic lines with a single copy of the transgene within one generation. Sequencing of each transgene insertion site revealed that they inserted as single copies with a preference for the introns of genes. The CAG promoter drove high levels of eGFP expression in brain, kidney, heart, and vasculature, making it very suitable for exploring the cardiovascular function of newly discovered genes. The pattern of eGFP expression was similar across five different F1transgenic lines, indicating that the expression of the transgene was independent of its chromosomal position. Thus lentiviral transgenesis provides a powerful tool for the production of transgenic inbred rats and will enhance the usefulness of this species in gene discovery and target validation studies.

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Alemayehu, Adamu, Laura Breen, and Morton P. Printz. "A new inbred Wistar-Kyoto rat substrain exhibiting apparent salt sensitivity and borderline hypertension." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 3 (September 1, 2002): H1181—H1190. http://dx.doi.org/10.1152/ajpheart.00187.2002.

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The normotensive Wistar-Kyoto (WKY) rat strain is a traditional control for the spontaneously hypertensive rat (SHR). We found trait differences between two inbred normotensive WKY strains, derived originally from different vendors, and compared these two strains from La Jolla-Taconic Farms (WKY/lj-tf) and La Jolla-Charles River (WKY/lj-cr) with the inbred SHR/lj-cr for cardiovascular, diurnal, and activity traits under normal and high (8%) NaCl diets. Marked genetic diversity was found between the two vendor-derived WKY. By using an extended study design and radiotelemetry, we compared WKY/lj-cr, WKY/lj-tf, and SHR/lj-cr with the following results: systolic pressure (120 ± 1, 133 ± 1, 168 ± 3 mmHg, respectively); diurnal variation in heart rate (ΔHR: 46 ± 3, 71 ± 4, 57 ± 2 beats/min, respectively); and salt sensitivity of arterial pressure (Δsystolic: 10 ± 1, 21 ± 1, 20 ± 1 mmHg, respectively). The WKY/lj-tf genotype apparently results in compromised control of arterial pressure and heart rate, especially during high NaCl intake, and greater susceptibility to high pressure (i.e., high NaCl-induced secondary changes). WKY/lj-tf thus constitutes a new inbred borderline hypertensive WKY substrain offering unique opportunities for genomic studies into the development of genetic hypertension.

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Cuenya, Lucas, Marta Sabariego, Rocío Donaire, Albert Fernández-Teruel, Carmen Torres, and Mauricio R. Papini. "Transfer across reward devaluation tasks in inbred Roman rat strains." Learning and Motivation 52 (November 2015): 22–31. http://dx.doi.org/10.1016/j.lmot.2015.08.003.

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Abbott, R. E., and D. Schachter. "Inheritance of salt-dependent hypertension in the inbred Dahl rat." Hypertension 24, no. 4 (October 1994): 506–11. http://dx.doi.org/10.1161/01.hyp.24.4.506.

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Bökenkamp, Regina, Adriana C. Gittenberger-De Groot, Conny J. Van Munsteren, Robert W. Grauss, Jaap Ottenkamp, and Marco C. Deruiter. "Persistent Ductus Arteriosus in the Brown-Norway Inbred Rat Strain." Pediatric Research 60, no. 4 (October 2006): 407–12. http://dx.doi.org/10.1203/01.pdr.0000238243.37116.a6.

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Biesiadecki, Brandon J., Paul H. Brand, Lauren G. Koch, Patricia J. Metting, and Steven L. Britton. "Phenotypic variation in sensorimotor performance among eleven inbred rat strains." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 5 (May 1, 1999): R1383—R1389. http://dx.doi.org/10.1152/ajpregu.1999.276.5.r1383.

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As a first step toward identifying the genes that determine sensorimotor ability (motor coordination) we subjected 11 inbred strains of rats to three different tests for this trait. Rats were tested at 13 wk of age to determine how long they could remain on 1) a rotating cylinder as the velocity of rotation increased every 5 s (1-direction rotation test), 2) a rotating cylinder that reversed direction every 5 s and increased velocity every 10 s (2-direction rotation test), and 3) a platform that was tilted 2° every 5 s from 22 to 47° (tilt test). On all three tests, rats of the PVG strain demonstrated the greatest sensorimotor ability. In contrast, rats of the MNS strain were most often represented among the group of strains that demonstrated the lowest performance on all tests. Considering all three tests, there was a 3- to 13-fold range in sensorimotor performance between the highest and lowest strains. This large divergence between the highest and lowest strains provides a genetic model that can be used to identify intermediate phenotypes and quantitative trait loci that contribute to sensorimotor ability.

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Basset, Alexandra, Dominique Laude, Stéphane Laurent, and Jean-Luc Elghozi. "Contrasting circadian rhythms of blood pressure among inbred rat strains." Journal of Hypertension 22, no. 4 (April 2004): 727–37. http://dx.doi.org/10.1097/00004872-200404000-00015.

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Yahata, T., T. Nagashima, M. Moriya, A. Kuroshima, F. Furuyama, and H. Nishino. "Improved cold-tolerance of the inbred heat-tolerant FOK rat." Pathophysiology 1 (November 1994): 215. http://dx.doi.org/10.1016/0928-4680(94)90447-2.

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Stanojević, Stanislava, Katarina Mitić, Vesna Vujić, Vesna Kovačević-Jovanović, and Mirjana Dimitrijević. "β-endorphin differentially affects inflammation in two inbred rat strains." European Journal of Pharmacology 549, no. 1-3 (November 2006): 157–65. http://dx.doi.org/10.1016/j.ejphar.2006.08.012.

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Sun, Q., and C. H. Turner. "Two Inbred Rat Strains That Differ Substantially in Hip Fragility." Calcified Tissue International 72, no. 4 (April 1, 2003): 498–504. http://dx.doi.org/10.1007/s00223-002-1040-7.

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Woon, Peng Y., Anne M. Curtis, Pamela J. Kaisaki, Karène Argoud, Karin J. Wallace, Marie-Thérèse Bihoreau, Garret A. FitzGerald, and Dominique Gauguier. "Genomic organization of the rat Clock gene and sequence analysis in inbred rat strains." Genomics 87, no. 2 (February 2006): 208–17. http://dx.doi.org/10.1016/j.ygeno.2005.10.006.

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Rose, Rajiv, Bijan S. Kheirabadi, and Harold G. Klemcke. "Arterial blood gases, electrolytes, and metabolic indices associated with hemorrhagic shock: inter- and intrainbred rat strain variation." Journal of Applied Physiology 114, no. 9 (May 1, 2013): 1165–73. http://dx.doi.org/10.1152/japplphysiol.01293.2012.

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We have previously shown interstrain variation (indicating a genetic basis), and intrastrain variation in survival time after hemorrhage (STaH) among inbred rat strains. To assist in understanding physiological mechanisms associated with STaH, we analyzed various arterial blood measures (ABM; pH, Paco2, oxygen content, sodium, potassium, glucose, bicarbonate, base excess, total CO2, and ionized calcium) in inbred rats. Rats from five inbred strains ( n = 8–10/strain) were catheterized and, ∼24 h later, subjected to a conscious, controlled, 47% hemorrhage. ABM were measured at the start (initial) and end (final) of hemorrhage. Inter- and intrainbred strain variations of ABM were quantified and compared, and correlations of ABM with STaH were determined. All final ABM values and some initial ABM values were different among strains. Most ABM changed (Δ) during hemorrhage, and these changes differed among strains ( P < 0.03). Some strain-dependent correlations ( r ≥0.7; P ≤ 0.05) existed between ΔABM and STaH (e.g., BN/Mcwi, ΔK+, r = −0.84). Dark Agouti rats (longest STaH) had the smallest ΔPaco2, ΔHCO3−, and Δbase excess, and the highest final glucose. High coefficients of variation (CVs, >10%), strain-specific CVs, and low intraclass correlation coefficients ( r I < 0.5) defined the large intrastrain ABM variation that exceeded interstrain variation for most ABM. These results suggest that some ABM (K+, Paco2, glucose, oxygen content) could predict subsequent STaH in an inbred rat strain-dependent manner. We speculate that whereas genetic differences may be responsible for interstrain variation, individual-specific epigenetic processes (e.g., DNA methylation) may be partly responsible for both inter- and intrastrain ABM variation.

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Avsaroglu, H., A. S. van der Sar, H. A. van Lith, L. F. M. van Zutphen, and L. J. Hellebrekers. "Differences in response to anaesthetics and analgesics between inbred rat strains." Laboratory Animals 41, no. 3 (July 1, 2007): 337–44. http://dx.doi.org/10.1258/002367707781282811.

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Differences in response to analgesic and anaesthetic drugs can partly be attributed to variations in the genetic background of experimental animals. This study was carried out to determine differences in the response of inbred rat strains to a selection of analgesics and drugs used in anaesthetic protocols. A cross between the most contrasting strains can then be phenotyped in future studies in order to localize quantitative trait loci (QTLs) involved in analgesic/anaesthetic drug sensitivity. Eight inbred strains ( n = 6 rats/strain) were selected for the study: the pigmented ACI, BN and COP strains and the albino F344, LEW, SHR, WAG and WKY strains. Each rat was injected intravenously with two analgesics (buprenorphine 0.05 mg/kg and nalbuphine 1 mg/kg) and three drugs used in anaesthetic protocols (propofol 25 mg/kg, medetomidine 50 μg/kg and ketamine 10 mg/kg), respectively, using a crossover design. Analgesic responses were assessed using an analgesiometric procedure. The sleep time of the rat and, where applicable, the interval between injection and loss of righting reflex were used to determine the anaesthetic response. Six out of eight strains responded significantly different from each other to the analgesic effect of buprenorphine with the ACI strain as hyper-responder. The tail withdrawal latency at 55°C of the F344 and WKY rats using buprenorphine was not significantly different from baseline tail withdrawal latencies. In this study, all strains were non-responsive to the analgesic effects of nalbuphine. The response to all three drugs used in anaesthetic protocols differed significantly among the strains. The F344 and BN strains were relatively resistant to the sedative effects of medetomidine. Use of ketamine was abandoned in the ACI and BN strains when the first two animals of both strains died soon after induction. With all three drugs the sleep time of albino rats was significantly longer compared with that of the pigmented ones. We conclude that the results from this study can be used in future studies where QTLs for the sensitivity to anaesthetic/analgesic drugs are localized.

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Waner, T., and A. Nyska. "Thyroxine (T4) and triiodothyronine (T3) levels in the Fischer 344 inbred rat." Laboratory Animals 22, no. 3 (July 1, 1988): 276–80. http://dx.doi.org/10.1258/002367788780746458.

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Plasma levels of T3 and T4 were measured in male and female Fischer 344 (F344/Cr1) inbred rats aged 10, 17, 30, 56, 80 and 106 weeks in order to document the hormone profile of this strain of rat. In general, levels of T4 were higher in males than in females. Levels of T3 were lower in females for the first 17 weeks, similar for rats of age 30 weeks, and thereafter higher in the females than the males. T4 concentration decline was age-associated in both sexes. T3 levels declined in the males only, but remained relatively constant in the females throughout their lifespan. Generally, T4/T3 ratios declined throughout the lifespan of the Fischer rat.

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32

Furuyama, F., and K. Ohara. "Genetic development of an inbred rat strain with increased resistance adaptation to a hot environment." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (October 1, 1993): R957—R962. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r957.

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The purpose of this study was to demonstrate resistance adaptation based on genotypic adaptation and to develop an inbred rat strain with genotypic resistance adaptation to a hot environment. Survival time (ST) at an ambient temperature (Ta) of 42.5 degrees C was determined without appreciable thermal damage. Rats with the longest ST were sibmated over 30 generations and designated FOK. The ST, evaporative water loss, and body water economy increased rapidly during the first 10-15 generations, followed by a more gradual increase. The FOK rat resisted a Ta of 42.5 degrees C for > 5 h; this ability was hereditary. Body size progressively decreased during the early generations. The ST was longer (P < 0.01) and evaporative water loss was significantly higher (P < 0.01) in the FOK rat compared with three other strains. Tail lengths in the FOK rat were slightly shorter than those of three controls (P < 0.01). The heat loss system in the FOK rat may depend on the ability to mobilize and evaporate body fluids efficiently. FOK rats can be used for phenotypic comparisons with other strains, as well as in molecular genetic studies on thermoregulation, osmoregulation, and resistance adaptation to heat using recombinant inbred and recombinant congenic lines.

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33

Klemcke, Harold G., Robert M. DeKroon, Mihaela Mocanu, Jennifer B. Robinette, and Oscar Alzate. "Cardiac mitochondrial proteomic expression in inbred rat strains divergent in survival time after hemorrhage." Physiological Genomics 45, no. 7 (April 1, 2013): 243–55. http://dx.doi.org/10.1152/physiolgenomics.00118.2012.

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We have previously identified inbred rat strains differing in survival time to a severe controlled hemorrhage (StaH). In efforts to identify cellular mechanisms and ultimately genes that are important contributors to enhanced STaH, we conducted a study to characterize potential differences in cardiac mitochondrial proteins in these rats. Inbred rats from three strains [Brown Norway/Medical College of Wisconsin (BN); Dark Agouti (DA), and Fawn Hooded Hypertensive (FHH)] with different StaH (DA = FHH > BN) were assigned to one of three treatment groups ( n = 4/strain): nonoperated controls, surgically catheterized rats, or rats surgically catheterized and hemorrhaged 24 h postsurgery. Rats were euthanized 30 min after handling or 30 min after initiation of a 26 min hemorrhage. After euthanasia, hearts were removed and mitochondria isolated. Differential protein expression was determined using 2D DIGE-based Quantitative Intact Proteomics and proteins identified by MALDI/TOF mass spectrometry. Hundreds of proteins (791) differed among inbred rat strains ( P ≤ 0.038), and of these 81 were identified. Thirty-eight were unique proteins and 43 were apparent isoforms. For DA rats (longest STaH), 36 proteins increased and 30 decreased compared with BN (shortest STaH). These 81 proteins were associated with lipid (e.g., acyl CoA dehydrogenase) and carbohydrate (e.g., fumarase) metabolism, oxidative phosphorylation (e.g., ubiquinol-cytochrome C reductase), ATP synthesis (F1ATPase), and H2S synthesis (3-mercaptopyruvate sulfurtransferase). Although we cannot make associations between these identified mitochondrial proteins and StaH, our data do provide evidence for future candidate proteins with which to consider such associations.

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Francisco, Nicole R., Christen M. Raymond, and Paul D. Heideman. "Short photoperiod inhibition of growth in body mass and reproduction in ACI, BUF, and PVG inbred rats." Reproduction 128, no. 6 (December 2004): 857–62. http://dx.doi.org/10.1530/rep.1.00390.

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Laboratory rats have been generally considered non-photoresponsive, but strains of laboratory rats have been found to be variable for this trait. Young males of both the Fischer (F344) and Brown Norway strains (BN) suppress reproductive development, food intake and body mass in short winter photoperiod (short days (SD); 8 h light:16 h darkness), and food restriction interacts with SD to enhance the effect of SD alone. Conversely, young male Harlan Sprague Dawley outbred rats, along with other outbred laboratory rats tested, have little or no response to SD except when unmasked by food restriction or other treatments, and have generally been considered nonphotoperiodic. In order to assess how widespread this trait might be among rat strains, and to test for uncoupling of reproductive and nonreproductive responses, we tested 3 additional inbred strains, including ACI, PVG and BUF rats, for photoresponsiveness and for unmasking of photoperiodic responses by food restriction. Young males of all three inbred strains exhibited photoresponsiveness in testis mass (5–20% lower in SD), seminal vesicle mass (20–50% lower in SD), and body mass (5–10% lower in SD). Food restriction also suppressed reproduction, but there was little or no interaction with the effects of photoperiod. The results are consistent with the hypothesis that laboratory rats are genetically variable for photoperiodism, and that photoresponsiveness may be widespread among inbred rat strains, as all five inbred strains tested have shown photoperiodic responses. The results are particularly important because standard research protocols may unknowingly manipulate this pathway in rats, causing unsuspected variability among or within studies.

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35

Baker-Herman, T. L., R. W. Bavis, J. M. Dahlberg, A. Z. Mitchell, J. E. R. Wilkerson, F. J. Golder, P. M. MacFarlane, J. J. Watters, M. Behan, and G. S. Mitchell. "Differential expression of respiratory long-term facilitation among inbred rat strains." Respiratory Physiology & Neurobiology 170, no. 3 (March 2010): 260–67. http://dx.doi.org/10.1016/j.resp.2009.12.008.

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36

Golder, Francis J., Andrea G. Zabka, Ryan W. Bavis, Tracy Baker-Herman, David D. Fuller, and Gordon S. Mitchell. "Differences in time-dependent hypoxic phrenic responses among inbred rat strains." Journal of Applied Physiology 98, no. 3 (March 2005): 838–44. http://dx.doi.org/10.1152/japplphysiol.00984.2004.

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Hypoxic ventilatory responses differ between rodent strains, suggesting a genetic contribution to interindividual variability. However, hypoxic ventilatory responses consist of multiple time-dependent mechanisms that can be observed in different respiratory motor outputs. We hypothesized that strain differences would exist in discrete time-dependent mechanisms of the hypoxic response and, furthermore, that there may be differences between hypoglossal and phrenic nerve responses to hypoxia. Hypoglossal and phrenic nerve responses were assessed during and after a 5-min hypoxic episode in anesthetized, vagotomized, and ventilated rats from four inbred strains: Brown Norway (BN), Fischer 344 (FS), Lewis (LW), and Piebald-viral-Glaxo (PVG). During baseline, burst frequency was higher in PVG than LW rats ( P < 0.05), phrenic burst amplitude was higher in PVG vs. other strains ( P < 0.05), and hypoglossal burst amplitude was higher in PVG and BN vs. FS and LW ( P < 0.05). During hypoxia, burst frequency did not change in BN or LW rats, but it increased in PVG and FS rats. The phrenic amplitude response was smallest in PVG vs. other strains ( P < 0.05), and the hypoglossal response was similar among strains. Short-term potentiation posthypoxia was slowest in FS and fastest in LW rats ( P < 0.05). Posthypoxia frequency decline was absent in PVG, but it was observed in all other strains. Augmented breaths were observed during hypoxia in FS rats only. Thus genetic differences exist in the time domains of the hypoxic response, and these are differentially expressed in hypoglossal and phrenic nerves. Furthermore, genetic diversity observed in hypoxic ventilatory responses in unanesthetized rats may arise from multiple neural mechanisms.

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37

Juberg, Daland R., Jenny T. Bond, and Wendell W. Weber. "N-acetylation of aromatic amines: genetic polymorphism in inbred rat strains." Pharmacogenetics 1, no. 1 (October 1991): 50–57. http://dx.doi.org/10.1097/00008571-199110000-00008.

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38

Bell, R. G., L. Adams, S. Coleman, D. Negrao-Correa, and T. Klei. "Brugia pahangi: Quantitative Analysis of Infection in Several Inbred Rat Strains." Experimental Parasitology 92, no. 2 (June 1999): 120–30. http://dx.doi.org/10.1006/expr.1999.4411.

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39

Löscher, Wolfgang, Sybille Cramer, and Ulrich Ebert. "Differences in Kindling Development in Seven Outbred and Inbred Rat Strains." Experimental Neurology 154, no. 2 (December 1998): 551–59. http://dx.doi.org/10.1006/exnr.1998.6948.

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40

van Wijngaarden, Peter, Douglas J. Coster, Helen M. Brereton, Ian L. Gibbins, and Keryn A. Williams. "Strain-Dependent Differences in Oxygen-Induced Retinopathy in the Inbred Rat." Investigative Opthalmology & Visual Science 46, no. 4 (April 1, 2005): 1445. http://dx.doi.org/10.1167/iovs.04-0708.

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41

Yahata, Takehiro, Fujiya Furuyama, Tomoaki Nagashima, Mitsuru Moriya, Kazue Kikuchi-Utsumi, Teruo Kawada, and Akihiro Kuroshima. "Thermoregulatory responses of the inbred heat-tolerant FOK rat to cold." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (August 1, 1999): R362—R367. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r362.

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The responses of inbred heat-tolerant FOK rats to cold were compared with those of Wistar King A/H (WKAH) and Std:Wistar (WSTR) strains. The fall of colonic temperature during cold exposure was unexpectedly smaller in FOK than in other groups, but the onset of shivering was delayed in FOK. Norepinephrine (NE)-induced in vivo oxygen consumption and the mitochondrial uncoupling protein 1 level of brown adipose tissue (BAT) were not different among the groups, but the cold-induced increases in in vivo oxygen consumption as well as plasma glycerol and free fatty acids were higher in FOK than in other groups. In vitro NE-induced oxygen consumption of BAT was less in FOK than WSTR, but not WKAH. The magnitude of the NE-induced increase in blood flow through BAT was higher in FOK than in other groups. These results suggest that FOK paradoxically have a high capacity for nonshivering thermogenesis in spite of their high capacity for heat tolerance, probably due to an increased lipid utilization and improved circulation of BAT.

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42

YAMADA, Takahisa, Daniel MORAREJO, Takashi AGUI, and Kozo MATSUMOTO. "Biochemical Polymorphisms in Long-Evans Cinnamon(LEC) Inbred Strain of Rat." Journal of Veterinary Medical Science 55, no. 3 (1993): 491–92. http://dx.doi.org/10.1292/jvms.55.491.

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43

Koster, Andries Sj, Leo Nieuwenhuis, and Ank C. Frankhuijzen-Sierevogel. "Comparison of microsomal drug-metabolizing enzymes in 14 rat inbred strains." Biochemical Pharmacology 38, no. 5 (March 1989): 759–65. http://dx.doi.org/10.1016/0006-2952(89)90228-1.

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44

Klemcke, Harold G., Bina Joe, Mariam L. Calderon, Rajiv Rose, Thomas Oh, James Aden, and Kathy L. Ryan. "Genetic influences on survival time after severe hemorrhage in inbred rat strains." Physiological Genomics 43, no. 12 (June 2011): 758–65. http://dx.doi.org/10.1152/physiolgenomics.00245.2010.

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To find a genetic basis for differential ability to survive severe hemorrhage, we previously showed eightfold differences in survival times among inbred rat strains. We assumed that rat strains had similar normalized blood volumes (NBV; ml/100 g body wt). As NBV might vary among strains and constitute one genetic variable affecting survival time to hemorrhage, in experiment 1 of the current studies we first measured total blood volumes and calculated NBV in specific inbred rat strains (Brown Norway/Medical College of Wisconsin, BN; Dark Agouti, DA; Fawn Hooded Hypertensive, FHH; Lewis, LEW; and Dahl Salt-Sensitive, SS) previously found to be divergent in survival time. NBV differed by 20% ( P < 0.01; BN > SS > FHH = LEW = DA) and had a heritability (h2) of 0.56. Hence, differential survival times in our previously published study might reflect strain-dependent differences in NBV. Then studies were conducted wherein rats were catheterized and, ∼24 h later, 47% of their blood volume was removed; these rats were observed for a maximum of 4 h. In experiment 2, blood volumes were measured the day prior to hemorrhage. Percent survival and survival time did not differ among strains. To obviate possible confounding effects of blood volume determination, in experiment 3 the average NBV for each strain was used to determine hemorrhage volumes. Percent survival ( P < 0.01) and survival times ( P < 0.001) were different with DA demonstrating the best (62.5%, 190 ± 29 min) and BN the worst (0%, 52 ± 5 min) survival responses. These data indicate that both blood volume and survival time after hemorrhage in rats are heritable quantitative traits, and continue to suggest that genetic assessment of these phenotypes might lead to novel therapeutics to improve survival to hemorrhage.

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45

Baker, John E., Eugene A. Konorev, Garrett J. Gross, William M. Chilian, and Howard J. Jacob. "Resistance to myocardial ischemia in five rat strains: is there a genetic component of cardioprotection?" American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (April 1, 2000): H1395—H1400. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1395.

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There is a need to develop new and more consistent animal models of cardioprotection. Traditionally, outbred dogs, rabbits, and rats have been studied. We determined resistance to ischemia in isolated hearts from inbred strains of rats. Hearts from inbred rats: SS/Mcw (Dahl S, Dahl salt-sensitive), DA/Hsd (Dark Agouti), LEW/Hsd (Lewis), and BN/SsN/Mcw (Brown Norway); and from an outbred rat: Hsd:WIST (Wistar) were subjected to 27 min of global, no-flow ischemia, followed by 3 h of reperfusion. Infarct size in the Brown Norway rat was 2.5 times less than that observed in the Dahl S rat, with the Dark Agouti, Lewis, and Wistar rats intermediate in response. Hearts from Brown Norway rats were also most resistant to ischemia in terms of postischemic enzyme leakage and contractile and vascular function compared with other strains. The average polymorphism rate between strains revealed that such strains were genetically diverse. This study demonstrates strain differences in resistance to myocardial ischemia, suggesting these rats could be used to study a genetic and/or environmental basis for these differences and to provide new animal models for the physiological study of cardioprotection.

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46

Zimmerman, Kurt A., Zhengqin Yang, Jeremie M. Lever, Zhang Li, Mandy J. Croyle, Anupam Agarwal, Bradley K. Yoder, and James F. George. "Kidney resident macrophages in the rat have minimal turnover and replacement by blood monocytes." American Journal of Physiology-Renal Physiology 321, no. 2 (August 1, 2021): F162—F169. http://dx.doi.org/10.1152/ajprenal.00129.2021.

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In this report, we performed parabiosis surgery on inbred Lewis rats and showed that rat kidney resident macrophages (KRMs), identified using our novel cross-species markers, are minimally dependent on peripheral blood input. Thus, for the first time, to our knowledge, we confirm that a hallmark of mouse KRMs is also present in KRMs isolated from another species.

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47

Sheppard, M. S., and R. M. Bala. "Profile of serum immunoreactive insulin-like growth factor I during gestation in Wistar rats." Canadian Journal of Physiology and Pharmacology 64, no. 5 (May 1, 1986): 521–24. http://dx.doi.org/10.1139/y86-086.

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It has been reported that there is a striking homology between the basic insulin-like growth factors (IGF) – somatomedins (SM) found in humans and rats. The radioimmunoassay (RIA) developed for the human hormone IGF-I (basic somatomedin, B-SM) can measure immunoreactive IGF-I in rat serum (IrIGF-I). Using this RIA, the profile of serum IrIGF-I was measured at each day of gestation in groups of inbred and Charles River Wistar rats. In each case IrIGF-I showed a gradual increase in early and mid gestation followed by a sharp decrease that occurred late in gestation to values 20–40% of control. The profile obtained from Charles River Wistars was shifted in time compared with the inbred group. Neither ovariectomy nor progesterone administration to ovariectomized nonpregnant animals altered serum MGF-I levels. Thus, although rat IGF-I and human IGF-I can be measured using the same assay, the changes that occur in gestation are in opposite directions.

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48

Konno, Toshihiro, Lea A. Rempel, M. A. Karim Rumi, Amanda R. Graham, Kazuo Asanoma, Stephen J. Renaud, and Michael J. Soares. "Chromosome-substituted rat strains provide insights into the genetics of placentation." Physiological Genomics 43, no. 15 (August 2011): 930–41. http://dx.doi.org/10.1152/physiolgenomics.00069.2011.

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The rat possesses a hemochorial form of placentation. Pronounced intrauterine trophoblast cell invasion and vascular remodeling characterize this type of placentation. Strain-specific patterns of placentation are evident in the rat. Some rat strains exhibit deep intrauterine trophoblast invasion and an expanded junctional zone [Holtzman Sprague-Dawley (HSD), Dahl salt sensitive (DSS)], whereas placentation sites of other rat strains are characterized by shallow invasion and a restricted junctional zone [Brown Norway (BN)]. In this report, we identified a quantitative trait that was used to distinguish strain-specific features of rat placentation. Junctional zone prolactin family 5, subfamily a, member 1 ( Prl5a1) transcript levels were significantly greater in BN rats than in HSD or DSS rats. Prl5a1 transcript levels were used as a quantitative trait to screen placentation sites from chromosome-substituted rat strains (BN chromosomes introgressed into the DSS inbred strain; DSS-BN panel). Litter size, placental weights, and fetal weights were not significantly different among the chromosome-substituted strains. Regulation of the junctional zone Prl5a1 transcript-level quantitative trait was multifactoral. Chromosome-substituted strains possessing BN chromosomes 14 or 17 introgressed into the DSS inbred rat strain displayed Prl5a1 transcript levels that were significantly different from the DSS pattern and more closely resembled the BN pattern. The in situ placental distribution of Prl5a1 mRNA and the structure of the junctional zone of DSS-BN17 rats mimicked that observed for the BN rat. Prl5a1 gene expression was also assessed in BN vs. HSD trophoblast stem cells and following reciprocal BN and HSD embryo transfer. Strain differences intrinsic to trophoblast and maternal environment were identified. In summary, we have identified chromosomes 14 and 17 as possessing regulatory information controlling a quantitative trait associated with rat placentation.

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PRAVENEC, MICHAL, VACLAV ZIDEK, ALENA MUSILOVA, VLADIMIR KŘEN, VLASTA BILA, and ROBERT DI NICOLANTONIO. "Chromosomal Mapping of a Major Quantitative Trait Locus Regulating Compensatory Renal Growth in the Rat." Journal of the American Society of Nephrology 11, no. 7 (July 2000): 1261–65. http://dx.doi.org/10.1681/asn.v1171261.

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Abstract. Despite extensive research conducted over the past century, the mechanisms of compensatory renal growth (CRG) remain a mystery. Insight into the mechanisms that regulate CRG might be gained by identifying genetic factors that influence this complex phenotype. In a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown Norway rat, a genome scan for quantitative trait loci (QTL) that regulate CRG was performed. The CRG score was expressed as a ratio of the weight of the remnant right kidney at 8 wk of age to the weight of the left kidney at 5 wk of age, both adjusted for body weight. QTL mapping was performed using Map Manager QT and the strain distribution patterns of more than 600 genetic markers. It was found that CRG after unilateral nephrectomy is a multifactorially determined trait with a substantial genetic component. The heritability of CRG approached 40%. Genome wide scan analysis revealed significant evidence of linkage to a region of rat chromosome 4 designated Crg 1 that accounted for more than 50% of the additive genetic variance of CRG in the recombinant inbred strains. The detection of a major QTL influencing CRG in the rat should provide new opportunities for identifying mechanisms that regulate this historically enigmatic phenomenon and may also have implications for research on the pathogenesis of end-stage kidney disease.

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50

Wang, C. G., G. DiMaria, J. H. Bates, R. D. Guttmann, and J. G. Martin. "Methacholine-induced airway reactivity of inbred rats." Journal of Applied Physiology 61, no. 6 (December 1, 1986): 2180–85. http://dx.doi.org/10.1152/jappl.1986.61.6.2180.

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Dose-response curves to inhaled aerosolized methacholine chloride (MCh) were obtained in anesthetized spontaneously breathing rats. Thirty rats (10/strain), randomly selected from highly inbred ACI, Lewis (L), and Brown Norway (BN) strains and 40 rats (20/strain) from similarly inbred Wistar-Furth (WF) and Buffalo (Buf) strains were studied. Airway responses were quantitated from changes in pulmonary resistance (RL) and airway reactivity was calculated as the dose of MCh required to increase RL to 150% (ED150RL) and 200% (ED200RL) of base line. There were no statistically significant differences in ED150RL and ED200RL among the five rat strains. Large interindividual variability was present as evidenced by 128-fold differences in ED150RL and ED200RL between the least and most sensitive animal of the same strain. In contrast, seven animals studied repeatedly on different days had values of ED150RL that differed by an average of only 2.9-fold (range 1.6–5.3). Thirteen rats that were studied on two occasions separated by an interval of 3 mo showed no systematic changes in airway reactivity. We conclude that airway reactivity to inhaled methacholine in anesthetized nose-breathing rats is not strain related, and despite animals of a given strain being genetically identical, the variability in airway reactivity within strains suggests that environmental rather than genetic factors are the major determinants of that reactivity.

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Journal articles on the topic 'Inbred rat'

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