Fattening responses to daily intervals of heat exposure in the Syrian hamster

Warm ambient temperature (38 degrees C) provided daily for one hr induced time-dependent changes in body weight and fat stores in the Syrian hamster. In animals held on 10-hr daily photoperiods and room temperature (23 degrees C), daily one-hour thermopulses at 8 and 20 hr after light onset stimulated increases in body weights and indices of body fat storage. Abdominal fat pad weights of these groups were twice those of untreated controls after 17 and 28 days of thermoperiodic treatments. On the other hand, daily thermopulses were completely ineffective at 0 and 16 hr after light onset. These results demonstrate that body fat stores may be influenced by a temporal interaction of environmental stimuli and implicate underlying circadian mechanisms in the regulation of body fat.     

Genetic studies of the Syrian hamster

A new mutant gene,anophthalmic white, is described for the Syrian hamster. The gene is inherited as a dominant to normal and, when homozygous, produces a characteristic syndrome of achromia and anophthalmia or microphthalmia. The heterozygote possesses white belly fur (instead of cream), a fine sprinkling of white hairs in the adult coat and a diminution of eye pigmentation. An occasional heterozygote may possess a small patch of unpigmented fur on the head or body. The new mutant does not appear to be linked with the gene forcream coat colour nor that forpiebald spotting. The significance of homologous mutants, with the above syndrome, in the mouse and hamster is briefly discussed.     

Genetic studies of the Syrian hamster

A new mutant allele of the Syrian hamster is described. It is inherited as an autosomal recessive and is probably an homologue of the gene for brown pigment, a mutational step which is known to occur in a number of rodent species. In animals homozygous for the mutant allele, all the normal black eumelanin is changed to brown. The new coat colour engendered in this manner is described in detail. The brown allele has been tested for linkage against the genes cream and ruby-eye but the results were negative.     

Chromosomal aberration,mutation and morphological transformation of Syrian hamster embryonic cells after exposure to methylnitrosocyanamide

Hamster embryonic fibroblasts were treated directly with various concentrations of methylnitrosocyanamide (MNC), a nitrosated product of methylguanidine (MG) or N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Then they were examined for chromosomal aberrations, morphological transformation and mutations resistant to 8-azaguanine (8AG) and 6-thioguanine (6TG). Direct treatment with 2 to 10 × 10^?6 M MNC caused a marked, dose-dependent appearance of 8AG- and 6TG-resistant mutations. The ability of MNC to induce mutations was similar to that of MNNG. Cultured embryonic fibroblasts in metaphase plates also showed a marked dose-dependent increase in chromosomal aberrations within 24 h after direct treatment with MNC of MNNG. Moreover, MNC and MNNG caused similar rates of morphological transformation.     

Experimental paracoccidioidomycosis in the Syrian hamster

Male hamsters (105) received intratesticular injection of suspension of a live yeast phase culture ofParacoccidioides brasiliensis and were sacrificed weekly during 20 weeks. Humoral immunity was studied by the agar-gel immunodiffusion (ID) and indirect immunofluorescence (IF) tests. Cell-mediated immunity was determined by the macrophage migration inhibition test in the presence of phytohemagglutinin (PHA) andParacoccidioides brasiliensis soluble antigen (PbAg). The morphology of the lesions was studied in the inoculation site, lymph nodes, lung, liver, spleen and kidneys.Disseminated paracoccidioidomycosis was observed in 100% of the animals after the first week. The lesions were initially made up of fungi surrounded by polymorphonuclear neutrophils and macrophages. Up to the 10th week the majority of the lesions appeared as compact confluent ephitelioid granulomas containing rare large fungi, some showing signs of degeneration. At this time, the specific antibody titers and the cellular immune response to PHA and PbAg were highest.From the 11th week on the granulomas became less compact, edematous with the epithelioid cells loosely arranged. This change was accompanied by an increase in the number of fungi showing reproductive activity and was associated with renal amyloidosis and progressive decline of cellular immune response both to PHA and PbAg. Contrariwise the titers of circulating antibodies were maintained.In the present model, disseminated paracoccidioidomycosis of the hamster was associated with depression of cellular immunity, change in the pattern of the granuloma, intense fungi proliferation and amyloidosis.     

Streptozotocin toxicity to cultured pancreatic islets of the Syrian hamster

Pancreatic islets of the Syrian golden hamster were maintained in culture for extended periods of time. Toxicity of streptozotocin in these cultures was evaluated by measurement of insulin secretion. Exposure of islets to 1 or 2 mM streptozotocin immediately following isolation resulted in a permanent and dose-related inhibition of insulin secretion. This was accompanied by islet disruption as observed by phase-contrast microscopy. Culture of islets for 24 hours before streptozotocin exposure afforded protection from toxicity. For example, exposure of freshly isolated islets to 2 mM streptozotocin resulted in complete destruction of beta cells, whereas islets similarly exposed after a 24 hr culture period continued to secrete insulin for many months. Islets maintained in culture for one week before exposure to 0.1–0.5 mM streptozotocin, however, became more sensitive than freshly isolated islets. Repeated weekly exposure of cultured islets to a non-toxic concentration (0.1 mM) resulted in sustained suppression of insulin secretion after 11 weeks.     

Immune response to acute virus infection in the Syrian hamster

Syrian hamsters show evidence of classical T-cell-mediated immune reactivity to acute virus infection as judged by primary foot pad swelling, kinetics of in vitro cytotoxic activity, and virus specificity of cytotoxic effector cells. In spite of this, no evidence of genetic restriction is observed among the variety of allodisparate inbred strains tested. This virus-induced, cell-mediated killing extends across strain barriers despite strong cellular and serologic alloreactivity among some of the strains utilized. To account for the apparent lack of genetic restriction, we currently favor the hypothesis that all hamsters examined thus far share at least one class I MHC antigen. Since these animals differ at hamster loci which elicit MLR, GVHR, acute SGR, CML, and alloantibody, we presume class II MHC polymorphism exists in this species. The presence of putative class II MHC polymorphism without detectable class I MHC polymorphism is unusual among mammals examined to date, and of unknown biologic significance.     

Assignment of the NRAS protooncogene to chromosome 12 of Syrian hamster by in situ hybridization.

The NRAS protooncogene codes for a GTP binding/GTPase p21 protein which resides on the inner surface of the plasma membrane. Using a human cDNA probe for NRAS, we have assigned the gene to Syrian hamster chromosome 12 with the most likely localization being 12qa5.     

Antigen-specific xenogeneic CTL activity in the Syrian hamster

Previous studies of the Syrian hamster have demonstrated a lack of cytotoxic T lymphocyte (CTL) activity in vaccinia virus-infected animals. Our laboratory has reexamined CTL activity in both the classical inbred strains, MHA, CB, and LSH, as well as the recently inbred strain MIT. Primary and secondary CTL specific for the immunizing antigen have been detected after in vitro culture in MIT but were not demonstrable in the classical strains. Only lymph node cells of the responding animal demonstrated this activity, spleen cells being phenotypically devoid of such a response. Identification of the cell responsible for cytolysis as a T cell was demonstrated by nylon wool nonadherence, specificity on Con A blasts, and the lack of surface immunoglobulin, as demonstrated by cell-sorter analysis.     

Naloxone antagonism of diazepam-induced feeding in the Syrian hamster

Three experiments investigated the effects of the intragastric administration of the benzodiazepine diazepam on feeding in non-deprived Syrian hamsters ($\text{mesocricetus auratus}$). In the first experiment diazepam (0, 0.5, 1.0, 2.0, and 4.0 mg/kg) produced dose dependant increases in feeding. 4.0 mg/kg of diazepam produced significantly more feeding than the other doses tested and the lowest dose tested (0.5 mg/kg) produced a significant increase in feeding. In the second experiment naloxone (10 mg/kg) partially antagonized the effect of 4 mg/kg of diazepam on feeding. In the third experiment the ability of naloxone (0.1, 1.0, 5.0, 10.0 or 20 mg/kg) to reduce feeding produced by either 4 mg/kg or 2 mg/kg of diazepam was tested. Naloxone partially antagonized the effects of 4 mg/kg of diazepam on feeding in a dose dependant manner. While 2 mg/kg of diazepam produced significantly less feeding than 4 mg/kg, naloxone did not antagonize the effect of 2 mg/kg on feeding. The results suggest that two mechanisms are involved in diazepam-induced feeding in hamsters. The high dose of diazepam may produce increased feeding by activating the endorphin system while the low dose of diazepam produces increased feeding via a naloxone insensitive mechanism.