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At least 19 recordsLinked to original sources
PubMed1984

Brain epinephrine systems: detailed comparison of adrenergic and noradrenergic metabolism, receptor number and in vitro regulation, in two inbred rat strains.

Epinephrine content and PNMT activity in medulla pons and hypothalamus of F344 inbred rats is from 3- to 8-fold higher than that of Buf inbred rats. These strain-dependent differences in brain adrenergic neurons are reciprocally related to altered alpha 1- adn alpha 2-adrenergic receptor density in PNMT-containing brain regions. Radioligand binding indices related to alpha 2-receptor function reveal that receptors may be 'desensitized' as well as 'down-regulated' in the strain with high PNMT activity (F344), and may be 'supersensitive' as well as 'up-regulated' in the strain with low PNMT activity (Buf). The association between epinephrine-containing neurons and alpha-adrenergic receptor regulation appears specific, since alpha-adrenergic receptor density and regulation in brain regions devoid of PNMT and epinephrine is similar in F344 and Buf rats. While noradrenergic metabolism in F344 rats is greater than that in Buf rats, this difference is generalized throughout the brain and, thus, bears no apparent relationship to the localized alterations in alpha-adrenergic receptor density. Moreover, beta-adrenergic receptor density in the 2 strains is similar in all brain regions. These data suggest that a significant proportion of alpha-adrenergic receptors in medulla-pons and hypothalamus are intimately related to and regulated by epinephrine-containing nerve endings.

Animals↗
PubMed1976

Spontaneous autoimmune thyroiditis in the BUF rat.

The inbred BUF rat develops autoimmune thyroiditis spontaneously. The incidence is related to the age of the animal and is increased by neonatal thymectomy and by treatment with methylcholanthrene. Autoantibodies to thyroglobulin can be demonstrated by indirect immunofluorescence and hemagglutination, but skin tests are negative. The "spontaneous" autoimmune disease may be due to the conjunction of an unusually vigorous immunological response to thyroglobulin and the loss of thymic suppressor function.

Animals↗
PubMed1980

Variable severity of glomerulonephritis in inbred rats infected with Trypanosoma rhodesiense. Correlation with immunoglobulin class-specific antibody responses to trypanosomal antigens and total IgM levels.

Five strains of inbred rats (ACI, BUF, F344, WF and WL) were infected with Trypanosoma rhodesiense and killed at 28 days for renal pathology and serological studies. The BUF strain demonstrated the most consistent and severe glomerulonephritis, accompanied by high titer IgM antibodies to trypanosomes and high total IgM levels. The WL strain demonstrated mild glomerulonephritis but prominent PAS (+) intracytoplasmic inclusions in proximal convoluted tubules, accompanied by low titer IgM antibodies and slightly elevated total IgM levels. All strains had low to medium titer IgG1 and IgGa antibodies to trypanosomes. Serial serologic studies in BUF rats showed peak titers of IgM, IgGa and IgG1 antibodies to trypanosomal antigens at 10 days. Immune complexes as measured by a C1q binding assay were elevated at 10 days, 3 days following the first detectable antibody responses, and remained so through the 30th day.

Animals↗
PubMed1983

Prolongation of rat kidney allografts by pretransplant administration of donor antigen extract or whole blood transfusion combined with a short course of cyclosporine.

The immunosuppressive effect of the combination of a three day course of cyclosporine with one i.v. injection of 3M KCL-extracted donor antigen or donor blood transfusion was tested across the strong histocompatibility barrier causing rejection within 8 days of kidney transplants from Buffalo (Buf, RT1b) to Wistar-Furth (WFu, RT1u) inbred rats. Administration of 10 mg/kg/day cyclosporine alone for three days (-1, 0, and 1) slightly prolonged graft survival time from 7 to 11 days. The combination of cyclosporine with donor Buf 3M KCl antigen or with a Buf blood transfurion administered one day prior to transplantation caused greater prolongation of graft survival--19 and 25 days, respectively. Neither third-party BN soluble antigen nor BN blood transfustions acted synergistically with cyclosporine to prolong Buf graft survival. Increasing doses of donor-soluble antigen up to an optimal dose of 5 mg proportionately prolonged graft survival; however, administration of 10 mg antigen was less effective than 5 mg. On the other hand, administration of 1 ml of donor blood achieved the maximal effect. Lymphocytes harvested ten days after transplantation from recipients that had received combined therapy with cyclosporine and donor 3M KCl antigen not only displayed specific unresponsiveness to donor stimulator cells in mixed lymphocyte culture, but also specifically suppressed the proliferative response of syngeneic, virgin WFu responder cells to allogeneic donor Buf but not to third-party BN cells. Furthermore, suppressor cell activity was suggested by diminished responses in an in vivo local adoptive mixed lymphocyte culture assay and by prolongation of Buf kidney survival following systemic adoptive transfer. These findings suggest that immunosuppression with cyclosporine permits induction of specific suppressor cells by 3M KCl donor antigen, resulting in specific unresponsiveness to allografts.

Animals↗
PubMed1984

Prolongation of allograft survival by repeated cycles of donor antigen and cyclosporine in rat kidney transplantation.

Combination therapy with a short course of cyclosporine (CsA) on the day prior to, to day of, and the day after transplantation and one dose of 5 mg 3M-KCl-extracted donor-soluble antigen (Ag) prolongs the survival of Buffalo (Buf, RT1b) kidney allografts in Wistar-Furth (WFu, RTu) inbred rats because of the induction of specific suppressor cells. Four systems were utilized to demonstrate suppressor cell activity in vivo. First, pooled lymphocytes from CsA-Ag-treated hosts suppressed the capacity of admixed, syngeneic WFu cells to display an in vivo mixed lymphocyte culture reaction toward donor Buf, but not third-party Brown-Norway (BN, RT1n), hosts. Second, systemic adoptive transfer two days prior to, or on the day of, transplantation of 5 x 10(8) putative suppressor cells harvested ten days after combined Ag-CsA treatment prolonged graft survival slightly but significantly from 7 to 9 days in virgin, secondary hosts. Third, admixture of 5 x 10(8) cells from Ag-CsA-treated hosts vitiated the capacity of 5 x 10(8) virgin WFu spleen cells to restore the capacity of recipients sublethally irradiated with 500 rads to reject. Buf allografts at 7.9 days rather than 16.7 days. Fourth, i.p. administration of low-dose cyclosphophamide (CY) 7 days after transplantation, a regimen known to inhibit suppressor cells, reduced the capacity of the Ag-CsA regimen to prolong graft survival. Two additional cycles of CsA therapy at 10-day intervals administered in an attempt to maintain T suppressor dominance over T helper cells prolonged median graft survival to 65 days. Similar prolongation was not achieved using donor blood transfusion as the immunogen, or using cycles of CsA alone. These findings suggest that 3M KCl donor antigen amplifies the induction of specific suppressor cells, and that CsA by virtue of helper T cell inhibition facilitates the establishment of suppressor cell dominance, eventually leading to host unresponsiveness.

Animals↗
PubMed1989

A genetic model for the control of host resistance to thermal injury.

The genetic control of resistance to a standardized model of severe thermal injury was studied using crosses between a resistant (BUF) and a susceptible (F344) strain of inbred rats; their reciprocal F1 hybrids and all eight possible backcross matings were examined for resistance to the same injury. Males were much more resistant than females, and none of the genes involved in resistance was linked to the major histocompatibility complex; there was also no evidence for a maternal effect upon the resistance of the offspring to thermal injury. The most parsimonious genetic model for host resistance to thermal injury based on the experimental data postulates control of resistance by two autosomal dominant genes and one X-linked recessive gene, with resistance factors being linearly additive.

Animals↗
PubMed1980

Depressed growth of Morris hepatomas in altitude- and heat-stressed but not in cold-stressed buffalo rats.

Female inbred BUF rats bearing Morris hepatomas 5123C, 5123D, 7795, and 7800 bilaterally in the femoral musculature were exposed for 3 weeks to ether 4,500-m simulated altitude or sea level or to an ambient temperature of either 7, 23, or 33 degrees C. Rats were given inoculations 12 days before these exposures. Tumor size, body weight, food consumption, and body temperatures were measured weekly in these treated rats and in normal rats. At time of killing, tumor mass, DNA synthesis (by [3H]thymidine incorporation), and respiration (by conversion of [1,4-14C]succinic acid to 14CO2) were measured in each of the 4 hepatoma lines, in the livers of normal and host rats, and in regenerated livers 10 days post 70% hepatectomy. Growths of all 4 tumors and regenerated livers were significantly impaired in rats stressed by exposure to altitude and heat but not to cold. Neither DNA synthesis nor respiration was altered in the hepatomas and livers by any environmental stress. The environmentally stressed rats gained weight at a slower rate and consumed less food than did their controls, but no differences were found in these variables for tumor-bearing and non-tumor-bearing rats. However, whereas the ratio of body weight gain to food consumed was reduced under the three stressful environments, that of tumor weight gain to food consumed was not altered by any environment. Host survivorship was not influenced by any of these effects.

Altitude↗
PubMed1979

Effect of inhibitory and stimulatory agents on protein synthesis in hepatomas and host livers of rats.

Female inbred BUF rats bearing intrahepatically transplanted hepatomas (5123 or 19) were subjected to acute exposure to a variety of hepatotoxic agents (actinomycin D, aflatoxin B1, CCl4, dimethylnitrosamine, ethionine, puromycin, or sparsomycin) or of stimulatory agents (hydrocortisone, phenobarbital, or whole-body X-ray). The responses in terms of changes in polyribosomes and protein synthesis (in vitro and in vivo) of host liver and hepatoma were evaluated. The responses of the host livers and hepatomas to the different agents varied. In general, the host livers responded much more than did the hepatomas. Of the two hepatomas, hepatoma 19 responded less (particularly in terms of polyribosome changes) than did hepatoma 5123. In a few experiments, different doses of actinomycin D, ethionine, or sparsomycin were used and in all instances the host livers responded more than did the hepatomas.

Animals↗
PubMed1993

The origin of the autoimmune disease-resistant LER rat: an outcross between the buffalo and autoimmune disease-prone Lewis inbred rat strains.

The Lewis (LEW) rat strain is highly susceptible to a large number of experimentally induced inflammatory and autoimmune diseases. The Lewis resistant (LER) rat strain, which reportedly arose as a spontaneous mutation in a closed colony of LEW rats, is resistant to many of these disorders. The mechanism of resistance is not yet clear. We report the analysis of 19 simple dinucleotide repeat polymorphisms in 13 rat strains including the LEW/N and LER/N rat strains. The LEW/N and LER/N alleles were the same in only 42% of cases. For all of the other polymorphisms, the LER/N and Buffalo (BUF/N) rat strain alleles were identical. These data provide evidence that the LER strain did not arise as a spontaneous mutation in the LEW strain but is the result of an outcross between the LEW and BUF rat strains. The LER rat strain is now a recombinant inbred rat strain. This information should facilitate the genetic analysis of the loci responsible for resistance to experimental autoimmune disease in the LER rat.

Alleles↗
PubMed2002

Myocardial function in rat genetic models of low and high aerobic running capacity.

We recently evaluated treadmill aerobic running capacity in 11 inbred strains of rats and found that isolated working left ventricular function correlated (r = 0.86) with aerobic running capacity. Among these 11 strains the Buffalo (BUF) hearts produced the lowest and the DA hearts the highest isolated cardiac output. The goal of this study was to investigate the components of cardiac function (i.e., coronary flow, heart rates, stroke volume, contractile dynamics, and cross-bridge cycling) to characterize further the BUF and DA inbred strains as potential models of contrasting myocardial performance. Cardiac performance was assessed using the Langendorff-Neely working heart preparation. Isolated DA hearts were superior (P < 0.05) to the BUF hearts for cardiac output (63%), stroke volume (60%), aortic +dP/dt (47%), and aortic -dP/dt (46%). The mean alpha/beta-myosin heavy chain (MHC) isoform ratio for DA hearts was 21-fold higher relative to BUF hearts. At the steady-state mRNA level, DA hearts had a fivefold higher alpha/beta-ratio than the BUF hearts. The mean rate of ATP hydrolysis by MHCs was 64% greater in DA compared with BUF ventricles. These data demonstrate that the BUF and DA strains can serve as genetic models of contrasting low and high cardiac function.

Adenosine Triphosphate↗
PubMed1983

Spontaneous diabetes mellitus syndrome in the rat. II. T lymphopenia and its association with clinical disease and pancreatic lymphocytic infiltration.

We have studied the occurrence of two phenotypic components (pancreatic lymphocytic infiltration [PLI] of the pancreas and T lymphocytopenia) of the spontaneous insulin-dependent diabetic syndrome (IDDM) in the progeny of hybrids obtained by crossing BB diabetic rats with rats of inbred strains differing from the BB rat at the major histocompatibility complex, RT1. Both PLI and T lymphopenia were seen in animals with all three possible genotypes in both (BUF x BB) and (LEW x BB) lines. PLI was seen in all IDDM animals. T lymphopenia was strongly associated with overt IDDM in both lines (chi 2 = 22.28, p = 0.00002 and chi 2 = 19.28, p less than 0.00001). In addition, T lymphopenia was associated with PLI with and without IDDM in both lines (chi 2 = 8.32, p = 0.0039 an chi 2 = 3.95, p = 0.0467). Not all animals exhibiting PLI without overt IDDM had depressed T cells. Not all animals with T lymphopenia had PLI with or without IDDM. In both lines, the overt IDDM occurred only in animals with at least one RT1 u haplotype derived from the BB rat, confirming our previously reported association of IDDM and RT1. We interpret this evidence to suggest that the overt IDDM syndrome requires one MHC-linked gene and at least two non-MHC-linked genes, which determine susceptibility to PLI and to circulating T lymphocyte depression.

Animals↗
PubMed1975

Spontaneous and methylcholanthrene-enhanced thyroiditis in BUF rats. I. The incidence and severity of the disease, and the genetics of susceptibility.

Virgin female Buffalo strain (BUF) rats that were treated with methylcholanthrene (MC) had a higher incidence of lymphocytic thyroiditis than untreated BUF rats. The degree of infiltration was also greater in MC-treated rats. The incidence of thyroiditis in retired breeder female BUF rats approached that found in MC-treated rats. The susceptibility to the effect of MC was not expressed in most F-1 hybrids of BUF and Lewis (LEW), a strain of rat that does not develop thyroiditis after treatment with MC.

Animals↗
PubMed1995

Type XI and II collagen-induced arthritis in rats: characterization of inbred strains of rats for arthritis-susceptibility and immune-responsiveness to type XI and II collagen.

To determine the relationship between susceptibility to bovine type XI and II (BXI and BII) collagen-induced arthritis, we immunized 14 inbred and one outbred strains of rats with BXI and BII. Susceptibility to BXI-arthritis corresponded largely with susceptibility, or resistance, to BII-arthritis. LEW, BB, WF, DA, and WKY were readily susceptible to BXI- and BII-arthritis. Likewise, BII-resistant F344 and BN rats were BXI-resistant. Some strains responded differently to BXI and BII. BUF and COP, which are moderately susceptible to BII, were BXI-resistant, whereas the BII-resistant rats, DA.1N and WF.1N, were partially susceptible to BXI. (F344 x BN) F1 hybrids responded to both collagens suggesting gene complementation. Arthritis occurred in all strains producing the highest titer antisera (LEW, WF and BB). Antibody responses to BXI and BII were generally commensurate within individual strains. DA were susceptible to arthritis but produced low levels of antibody comparable to BN rats which were arthritis-resistant. BXI and BII-susceptibility was variable in rats producing intermediate antibody responses. Antibodies to RXI were detected in all BXI-immunized rats, whereas antibodies to RV and RII were uniformly weaker. DTH to RXI and RII was strong in both groups of rats, correlating poorly with arthritis and antibody responses. These studies show that phenotypic susceptibility to BXI- and BII-arthritis are largely concordant among inbred rat strains but clear differences exist in certain strains; multiple genes are likely involved.

Animals↗
PubMed1981

Immunogenetic control of experimental type II collagen-induced arthritis. I. Susceptibility and resistance among inbred strains of rats.

Seven inbred rat strains were tested for susceptibility to experimental type II collagen-induced arthritis and for development of cellular immunity to type II collagen by delayed hypersensitivity skin testing. WF (RT1u), LEW (RT1l), and DA (RT1a) were the most susceptible of the strains tested with respect to incidence (greater than 95%) and severity of disease. LEW and DA were strongly skin test reactive to calf type II collagen. BUF (RT1b) developed moderate skin test responses to calf type II collagen and showed low susceptibility to collagen arthritis (1/8). MAXX (RT1n), LEW.B3 (RT1nvl), and AUG (RT1c) were not susceptible to collagen arthritis and showed negative to very weak skin test responses to type II collagen. Disease susceptibility was inherited as a dominant trait in the F1 progeny of (WF X LEW.B3) matings. These data suggest that clinical expression of experimental collagen-induced arthritis and immune responsiveness to type II collagen are controlled in part by genes within or closely linked to the rat major histocompatibility complex--RT1.

Animals↗
PubMed1983

Anti-idiotypic immunity and autoimmunity. II. Idiotypic determinants of autoantibodies and lymphocytes in spontaneous and experimentally induced autoimmune thyroiditis.

In a previous report, it was demonstrated that heterologous anti-idiotypic antibodies to autoantibodies against rat thyroglobulin (ART) were capable of inhibiting the in vitro binding between ART and rat thyroglobulin. It has also been shown that repeated injections of anti-idiotypic antibodies into Buffalo (BUF) rats with spontaneous autoimmune thyroiditis were followed by a significant decrease in the levels of circulating ART. In this report, cross-reacting idiotypic determinants, detectable by rabbit anti-idiotypic antibodies to ART, are shown to also be present on ART from rats with experimentally induced autoimmune thyroiditis. In addition, antibodies to rat thyroglobulin from animals of various strains and species are shown to also express idiotypes cross-reacting with those of spontaneous ART of BUF rats. Finally, it is reported that idiotypic determinants similar to those of circulating ART are present on spleen lymphocytes from rats with autoimmune thyroiditis.

Animals↗
PubMed1993

Structure of the vitreoretinal border region in spontaneously hypertensive rats (SHR rats).

The morphology of the vitreoretinal border region, also termed the inner limiting membrane, was studied in spontaneously hypertensive rats (SHR rats), in Wistar Kyoto rats (WKY rats), and in Buffalo rats (BUF rats). The region was examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) in order to visualize a possible increase in thickness with raised arterial pressure. The median thickness of the lamina densa in TEM in the three groups varied from 34 to 68 nm. In hypertensive SHR rats the lamina densa showed thickening up to the 10th month and was unchanged thereafter. The same pattern was shown in WKY rats, although the thickness increased also after the tenth month in these controls. In BUF rats, however, the lamina densa decreased in thickness with age. The median thickness of the whole vitreoretinal border region varied between: SHR rats: 42 and 84 nm (SEM) and 51 and 127 nm (TEM); WKY rats: 84 nm (SEM) and 51 and 68 nm (TEM); BUF rats: 42 nm (SEM) and 34 and 68 nm (TEM). SHR rats showed in SEM an increase in thickness with age. In TEM, however, only one very old hypertensive rat had a thickened vitreoretinal border region. In WKY rats both SEM and TEM showed an increase in thickness with age, whereas BUF rats showed a decrease. Fundus photographs disclosed narrow, straight and irregular retinal arterioles in hypertensive SHR rats. Light microscopy of older SHR rats demonstrated retinal degeneration from the outer photoreceptor layer to the inner nuclear layer. This was also found in some of the older WKY rats.

Animals↗
PubMed1977

Cellular components of allograft rejection: identity, specificity, and cytotoxic function of cells infiltrating acutely rejecting allografts.

Functioning mononuclear cells have been harvested from heterotopic rat cardiac allografts during maximal transplant cellular infiltration. T cells, identified by a T cell-specific absorbed rabbit anti-rat brain serum, constituted two-thirds of the total cells recovered. Approximately 20% of the infiltrating cells bear and synthesize surface immunoglobulin. Macrophages, identified by latex ingestion and morphologic and cytochemical techniques, comprise 9% of the graft infiltrate. Donor-specific cytotoxic T lymphocytes are concentrated within the graft. A separate population of Fc receptor-positive recovered cells mediate antibody-dependent LMC (Ab-LMC). Neither effector cell was adherent or phagocytic. These studies have conclusively established that cytotoxic T lymphocytes accumulate within rejecting allografts; however, the enriched presence of cytotoxic T cells within the grafts is not fully dependent upon antigen recognition per se, since Lew animals grafted with both BN and BUF hearts have Lew anti-BN and Lew anti-BUF killer cells in each graft.

Animals↗
PubMed1975

Spontaneous and methylcholanthrene-enhanced thyroiditis in BUF rats. II. Induction of experimental autoimmune thyroiditis without completed Freund's adjuvant.

The immunization of Buffalo strain (BUF) rats with rat thyroid extract and Bordetella pertussis vaccine without complete Freund's adjuvant resulted in experimental autoimmune thyroiditis (EAT) in 90% of the rats by the 10th day after immunization. The treatment did not elicit thyroiditis in Lewis strain (LEW) rats. This susceptibility to the induction of EAT without the use of complete Freund's adjuvant was inherited by F1 hybrids of BUF and LEW. Neither histamine sensitizing factor from B. pertussus nor Escherichia coli vaccine substitute for whole pertussis vaccine.

Animals↗