Colony Of Rats Research Articles

Devices for handling small mammals in laboratory conditions.

Wild rodents, and especially rats, are significantly more difficult to handle, maintain and breed than laboratory rats and mice. They can be characterized as more skittish, neophobic and aggressive. While establishing a breeding colony of wild Norwegian rats (Rattus norvegicus) I developed some helpful devices and I will describe them here. In this paper I also describe the techniques for transporting animals between their home cages, separating them inside cages, and catching individuals that escape. These devices do not require any home cage modification. They may be modified for size. With size modification these devices may be used for handling animals in any type of laboratory cages. They may be used with all species of small mammals, for example, mice, gerbils, hamster, and opossums. They prove especially helpful when physical contact with humans is a problem (e.g. SPF conditions of breeding, and behavioral procedures that do not allow handling).

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Carcinogenicity of Aspartame in Rats Not Proven

Carcinogenicity of Aspartame in Rats Not Proven

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Growth and reproductive problems in a colony of laboratory rats

Growth and reproductive problems in a colony of laboratory rats

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Characterization of central and peripheral components of the hypothalamus–pituitary–adrenal axis in the inbred Roman rat strains

Several studies performed in outbred Roman high- and low-avoidance lines (RHA and RLA, respectively) have demonstrated that the more anxious line (RLA) is characterized by a higher hypothalamic-pituitary-adrenal (HPA) response to certain stressors than the less anxious one (RHA). However, inconsistent results have also been reported. Taking advantage of the generation of an inbred colony of RLA and RHA rats (RHA-I and RLA-I, respectively), we have characterized in the two strains not only resting and stress levels of peripheral HPA hormones but also central components of the HPA axis, including CRF gene expression in extra-hypothalamic areas. Whereas resting levels of ACTH and corticosterone did not differ between the strains, a greater response to a novel environment was found in RLA-I as compared to RHA-I rats. RLA-I rats showed enhanced CRF gene expression in the paraventricular nucleus (PVN) of the hypothalamus, with normal arginin-vasopressin gene expression in both parvocellular and magnocellular regions of the PVN. This enhanced CRF gene expression is not apparently related to altered negative corticosteroid feedback as similar levels of expression of brain glucorticoid and mineralocorticoid receptors were found in the two rat strains. CRF gene expression tended to be higher in the central amygdala and it was significantly higher in the dorsal region of the bed nucleus of stria terminalis (BNST) of RLA-I rats, while no differences appeared in the ventral region of BNST. Considering the involvement of CRF and the BNST in anxiety and stress-related behavioral alterations, the present data suggest that the CRF system may be a critical neurobiological substrate underlying differences between the two rat strains.

A brief biography of Bruce Merrifield: His life and legacy

A brief biography of Bruce Merrifield: His life and legacy

Biochemical, Pathological, and Skeletal Improvement of Mucopolysaccharidosis VI After Gene Transfer to Liver but Not to Muscle

Mucopolysaccharidosis VI (MPS VI) is caused by deficient activity of arylsulfatase B (ARSB), resulting in intralysosomal storage of dermatan sulfate (DS) and multisystem disease without central nervous system involvement. After gene transfer, muscle or liver can theoretically be converted into factories for systemic ARSB secretion, leading to uptake by non-transduced cells. We have injected newborn MPS VI rats and cats with adeno-associated viral (AAV) vectors expressing ARSB under the control of liver-specific, muscle-specific, or universally active promoters. After systemic or intramuscular (IM) administration of AAV, therapeutic levels of circulating ARSB are achieved, resulting in skeletal improvements and significant decrease in glycosaminoglycan (GAG) storage, inflammation and apoptosis (despite a neutralizing immune response to ARSB in MPS VI rats). In addition, we have observed wide-spread dissemination of vector after IM AAV administration. This results in secretion of therapeutic levels of ARSB when the universally active cytomegalovirus (CMV) but not the muscle-specific muscle creatine kinase (MCK) promoter is used, suggesting that transduction of extramuscular sites rather than enzyme secretion from muscle occurs after muscle ARSB gene transfer. We conclude that AAV-mediated expression of ARSB from liver represents a feasible therapeutic strategy for MPS VI, potentially avoiding multiple infusions of costly recombinant enzyme associated with enzyme replacement therapy.

Evaluation of evidence for infection as a mode of action for induction of rat lymphoma

The European Food Safety Authority (EFSA) released a 2006 report questioning the relationship of aspartame exposure with increased incidence of lymphomas/leukemias in a European Ramazzini Foundation (ERF) rat study. The EFSA report suggested that the lymphoma/leukemia findings were most likely explained by infection in the rat colony. The ERF has also conducted the only available long-term oral study of methyl tertiary-butyl ether (MTBE). Thus, using the EFSA report as support, some have now raised questions about the human relevance of MTBE-associated hemolymphoreticular tumors reported by the ERF in female rats as well as whether their incidence was elevated above background levels. In this report, we discuss the hypothesized mode of action (MOA) of infection-induced lymphoma and its relevance to MTBE-associated lymphomas. We address the relationship of rat strain and study duration to lymphoma susceptibility and review evidence of low background rates of this tumor in control animals at the ERF, similar survival rates for female rats at the ERF and National Toxicology Program (NTP), and chemical- and gender-specificity of tumor induction for this type of tumor in studies at the ERF. We find that the background incidence of hemolymphoreticular tumors in female rats in the MTBE study is consistent with contemporaneous studies at the ERF and that there is an exposure-related effect, which is unlikely to be due to infections. We examine more recent tumor classification schemes for lymphomas, which support the combination of lymphoblastic leukemias and lymphomas reported by Belpoggi et al. ([1995] Toxicol Ind Health 11:119-149; [1998] Eur J Oncol 3:201-206).

Sanitary profile in mice and rat colonies in laboratory animal houses in Minas Gerais: I - Endo and ectoparasites

The sanitary conditions of 13 animal houses in nine public institutions in Minas Gerais, and the presence of endo and ectoparasites of mice and rats colonies kept in these facilities were evaluated. Data about barriers to prevent the transmission of diseases and a program of sanitary monitoring were obtained through a questionnaire and local visit. Parasitological methods were performed for diagnosing mite, lice, helminthes, and protozoa parasites in 344 mice and 111 rats. Data have shown that the majority of the animal houses had neither proper physical environment nor protection barriers to prevent the transmission of infections. Parasitological results have shown that only one animal house (7.7%) had parasite free animals, whereas the others have presented infected animals and the prevalences of parasites in the mice colonies were: Myobia musculi (23.1%); Myocoptes musculinus (38.5%); Radfordia affinis (15.4%); Syphacia obvelata (92.3%); Aspiculuris tetraptera (23.1%); Hymenolepis nana (15.4%); Spironucleus muris (46.2%); Giardia muris (46.2%); Tritrichomonas muris (53.8%); Trichomonas minuta (61.5%); Hexamastix muris (7.7%); and Entamoeba muris (84.6%). As for the rat colonies, the prevalences were: Poliplax spinulosa (8.1%); Syphacia muris (46.2%); Trichosomoides crassicauda (28.6%); Spironucleus muris (85.7%); Tritrichomonas muris (85.7%); Trichomonas minuta (85.7%); Hexamastix muris (14.3%) and Entamoeba muris (85.7%).

Of mighty mice and diabetic men: animal models of islet dysfunction

Of mighty mice and diabetic men: animal models of islet dysfunction

Islet gene expression and function in type 2 diabetes; studies in the Goto‐Kakizaki rat and humans

Defective beta-cell function with resulting impairment of glucose-stimulated insulin release is a critical factor in the pathogenesis of type 2 diabetes. Accumulated studies in pancreatic islets of the spontaneously diabetic Goto-Kakizaki (GK) rat suggest that this is a useful animal model of type 2 diabetes. The GK rat is non-obese, and abnormal glucose regulation develops early in life in association with impaired insulin secretion. There are some differences in islet morphology and function reported between different GK rat colonies. In addition to reduction of beta-cell mass, a number of beta-cell defects have been described with possible relevance for the reduced insulin secretion. Interestingly, some of these defects have also been shown in isolated islets from type 2 diabetic humans. The polygenic nature of diabetes heredity in the GK rat may well resemble the genetic basis in the majority of patients with type 2 diabetes. Here, we review studies concerning beta-cell function and islet gene expression in the GK rat and compare it with the limited number of investigations on similar topics in isolated islets from patients with type 2 diabetes.

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Endocrine-Related Resources from the National Institutes of Health

Prevalence and Genetic Properties ofSalmonella entericaSerovar Typhimurium Definitive Phage Type 104 Isolated fromRattus norvegicusandRattus rattusHouse Rats in Yokohama City, Japan

Salmonella enterica serovar Typhimurium was isolated from the intestinal contents of Rattus rattus and Rattus norvegicus house rats captured at two buildings, designated buildings J and YS, in Yokohama City, Japan. From October 1997 to September 1998, 52 of 339 (15.3%) house rats were found to carry Salmonella serovar Typhimurium definitive phage type 104 (DT104). In building J, 26 of 161 (16.1%) house rats carried DT104 over the 1-year study period, compared to 26 of 178 (14.6%) rats in building YS. The isolation rates of DT104 from R. rattus and R. norvegicus were similar in the two buildings. Most DT104 strains from building J (24 of 26) showed resistance to ampicillin, chloramphenicol, streptomycin, sulfisoxazole, and tetracycline and contained both the 1.0- and 1.2-kbp integrons, carrying genes pse1, pasppflo-like, aadA2, sulI, and tet(G). All DT104 strains from building YS were resistant to ampicillin and sulfisoxazole, and had the 1.2-kbp integron carrying pse1 and sulI. Cluster analysis of pulsed-field gel electrophoresis patterns of BlnI-digested DT104 DNAs showed that 22 of 26 DT104 strains from building J and 24 of 26 strains from building YS could be grouped into separate clusters each specific for the building origin. These results indicated that DT104 strains were prevalent in house rat colonies in each building and suggest that house rats may play an important role in the epidemiology of DT104.

The effect glucocorticoids on aggressiveness in established colonies of rats

It was repeatedly shown that glucocorticoids increase aggressiveness when subjects are socially challenged. However, the interaction between challenge exposure and glucocorticoid effects was not investigated yet. We studied this interaction by assessing the effects of glucocorticoids in established colonies of rats, i.e. in rats that were not exposed to an acute social challenge. Aggressiveness was high immediately after colony formation but decreased sharply within 4 days and remained stable thereafter. Mild dominance relations were observed in 11 colonies (65%). Approximately three weeks after colony formation, rats remained undisturbed or were injected with vehicle or corticosterone. Routine colony life was followed for 1h after treatments. Injections per se induced a mild and transient behavioral activation: resting was reduced, whereas exploration, social and agonistic interactions were increased. The change lasted about 15min. Corticosterone--although plasma corticosterone levels were increased--had no specific effect, as the behavior of vehicle- and corticosterone-treated rats was similar. Social rank had a minor impact on the results. In contrast, the pro-aggressive effects of corticosterone were robust under conditions of social challenge and were maintained after repeated exposure to aggressive encounters. It occurs that an acute increase in glucocorticoids promotes social challenge-induced aggressiveness, but does not increase aggressiveness under routine conditions. We hypothesize that the pro-aggressive effects of glucocorticoids develop in conjunction with challenge-induced neuronal (e.g. monoaminergic) activation.