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PubMed2006

Selective extra-dimensional set shifting deficit in a knock-in mouse model of Huntington's disease.

People with early-stage Huntington's disease have been found to have a specific deficit in performing an extra-dimensional shift. To date no evidence of this deficit has been identified in transgenic or knock-in rodent models of the disease. The aim of the present paper then, was to test whether homozygous knock-in mice derived from the Hdh(CAG(150)) mouse line were impaired in any of five 2-choice discrimination tasks (simple, compound, compound reversal, intra-dimensional shift and extra-dimensional shift), and whether these mice were impaired at recalling these tasks on the following day. On the extra-dimensional shift task the Hdh(CAG(150)) homozygous mice required a greater number of trials to reach criteria than mice and the percentage of correct choices within the trials was also significantly reduced compared with the animals. For the recall tasks, a deficit for recalling the compound reversal test was found in the Hdh(CAG(150)) homozygous mice for both number of trials required to reach criteria and percentage of correct choices within the trials. Recall for the intra-dimensional shift task was also impaired in these animals when measured by the percentage of correct choices. Our results demonstrate a pronounced deficit in the Hdh(CAG(150)) mice not only on extra-dimensional shift performance in agreement with human studies, but also on recall tasks for both the compound reversal and the intra-dimensional shift tasks.

Animals↗
PubMed2006

Efficacy of IL-13 neutralization in a sheep model of experimental asthma.

IL-13 contributes to airway hyperresponsiveness, mucus secretion, inflammation, and fibrosis, suggesting that it plays a central role in asthma pathogenesis. Neutralization of IL-13 with sIL-13Ralpha2-Fc (sIL-13R) reduces allergen-induced airway responses in rodent models of respiratory disease, but its efficacy in a large animal model has not been previously reported. In this study, we determined whether two different strategies for IL-13 neutralization modified experimental asthma in sheep. Sheep with natural airway hypersensitivity to Ascaris suum antigen were treated intravenously either with sIL-13R, a strong antagonist of sheep IL-13 bioactivity in vitro, or with IMA-638 (IgG1, kappa), a humanized antibody to human IL-13. Higher doses of IMA-638 were used because, although it is a potent antagonist of human IL-13, this antibody has 20 to 30 times lower binding and neutralization activity against sheep IL-13. Control animals received human IgG of irrelevant specificity. Sheep were treated 24 h before inhalation challenge with nebulized A. suum. The effects on antigen-induced early and late bronchial responses, and antigen-induced hyperresponsiveness, were assessed. Both sIL-13R and IMA-638 provided dose-dependent inhibition of the antigen-induced late responses and airway hyperresponsiveness. The highest dose of IMA-638 also reduced the early phase response. These findings suggest that IL-13 contributes to allergen-induced airway responses in this sheep model of asthma, and that neutralization of IL-13 is an effective strategy for blocking these A. suum-induced effects.

Amino Acid Sequence↗
PubMed1992

Quinolinate in brain and cerebrospinal fluid in rat models of congenital hyperammonemia.

Children with inborn errors of urea synthesis who survive neonatal hyperammonemic coma commonly exhibit cognitive deficits and neurologic abnormalities. Yet, there is evidence that ammonia is not the only neurotoxin. Hyperammonemia appears to induce a number of neurochemical alterations. In rodent models of hyperammonemia, uptake of L-tryptophan into brain is increased. It has been reported that in an experimental rat model of hepatic encephalopathy, in the ammonium acetate-injected rat, and in patients with hepatic failure and inborn errors of ammonia metabolism, quinolinate, a tryptophan metabolite, is increased. Elevations in quinolinate are of particular concern, as quinolinate could excessively activate the N-methyl-D-aspartate subclass of excitatory amino acid receptors, thereby causing selective neuronal necrosis. We sought to identify an animal model that would replicate the increases in quinolinate that have been associated with hyperammonemia in humans. Levels of quinolinate were measured in hyperammonemic urease-infused rats and ammonium acetate-injected rats. In the urease-infused rat, brain tryptophan was doubled, and serotonin and its metabolite 5-hydroxyindoleacetic acid were significantly increased. Yet, despite the increase in tryptophan and evidence for increased metabolism of tryptophan to serotonin, there were no observed increases of quinolinate in brain, cerebrospinal fluid, or plasma. In the ammonium acetate-injected rat, significant increases of 5-hydroxyindoleacetic acid in cerebral cortex were also observed, but quinolinate did not change in cerebrospinal fluid or cerebral cortex. In summary, we were unable to demonstrate an increase of quinolinate in brain or cerebrospinal fluid in these rat models of hyperammonemia.

Acetates↗
PubMed2004

An amphibian model to test the effects of xenobiotic chemicals on development of the hematopoietic system.

A number of manmade chemicals have deleterious effects on the developing immune system. Very few assay systems are available to study the effects of xenobiotics on hematopoietic stem cells. In rodent models, assays require exposure of pregnant females and analysis of the hematopoietic potential of stem cells from the offspring. These models are less relevant to lower vertebrates such as fish or amphibians where exposure of embryos is direct. To overcome this problem, an amphibian model was developed. Diploid (2N) embryos (16-20 h of age) of the South African clawed frog, Xenopus laevis, were exposed to 10 microg/ml diazinon or 10(-6) M lead acetate for 2 h. After 2 h, the ventral blood island (VBI) was transplanted from a chemically treated or untreated control embryo to an untreated triploid (3N) host embryo. After 55 d, the contribution of the donor VBI-derived stem cells to populations in the blood, thymus, and spleen was assessed by flow cytometry. Diazinon, but not lead acetate, interfered with the ability of transplanted stem cells to contribute to hematopoiesis. Because amphibian embryos are very sensitive indicators of the toxic effects of chemicals, this VBI assay could be employed to test any toxic chemical that is suspected of having a negative effect on development of the hematopoietic system.

Animals↗
PubMed1971

Testosterone metabolism in the androgen-insensitive rat: a model for testicular feminization.

Although it has long been known that the lack of androgen dependent differentiation in patients with testicular feminization is secondary to end organ insensitivity, the molecular basis of this genetic disorder has not been elucidated. In the present report a rodent model for testicular feminization is described. The Stanley-Gumbreck pseudohermaphroditic rat has an inherited disorder characterized by a female phenotype, a male genotype and tissue insensitivity to androgens. Even though male differentiation does not occur when these animals are treated with physiologic doses of testosterone, some androgen dependent growth is evident when 100-fold larger doses of testosterone are given. Studies of androgen metabolism in the psuedohermaphroditic animals indicate that testosterone transport and metabolism to dihydrotestosterone are normal. However, intranuclear retention of dihydrotestosterone is defective. These findings suggest that the androgen insensitivity of the pseudohermaphroditic rat is due to an inherited abnormality of a regulatory protein which renders the nucleus of the cell incapable of concentrating androgens at their proposed intracellular site of action. The pseudohermaphroditic rats also have a defect of testicular and adrenal steroid synthesis in addition to the androgen insensitivity. The relation of these two abnormalities in rat and in man are discussed.

Adrenal Glands↗
PubMed1998

Animal behavior models. Increased sensitivity to stressors and other environmental experiences after prenatal cocaine exposure.

Neural compensations occurring after prenatal cocaine exposure may often permit some functional recovery, although the cost of this reorganization may be a decrease in adaptability. As we have seen in our rodent model of prenatal cocaine exposure, latent deficits may become unmasked when offspring are exposed to cognitive and environmental demands and stressors. In adolescence and adulthood, offspring exposed gestationally to cocaine exhibit characteristic decreases in stress-induced immobility along with increases in aggression under the demands of social competition. Recently, we observed that cocaine-exposed offspring are also unusually sensitive to the long-term effects of early manipulation (noninvasive heart rate testing at 16 days of age). When tested in adulthood, cocaine-exposed offspring not receiving this early experience exhibited less immobility when tested in the presence of intermittent footshock or when subsequently examined in an open field as well as more locomotion in the open field than control offspring, findings reminiscent of previous work. By contrast, these effects were normalized (shock-induced immobility) or reversed (open field immobility and locomotion) in cocaine-exposed animals given the early experience. This marked susceptibility to the effects of early manipulation was less evident in control offspring and even in a group of stunted nutritional controls. Thus, cocaine-exposed offspring may exhibit increased sensitivity not only to environmental demands and stressors, but also to the potential moderating or beneficial effects of early experiences.

Aging↗
PubMed2005

Temporary focal ischemia in the mouse: technical aspects and patterns of Fluoro-Jade evident neurodegeneration.

Animal models of cerebral infarction are crucial to understanding the mechanisms of neuronal survival following ischemic brain injury and to the development of therapeutic interventions for victims of all types of stroke. Rodents have been used extensively in such research. One rodent model of stroke utilizes either permanent or temporary occlusion of the middle cerebral artery (MCAO) to produce ischemia. Since the development of an endovascular method for this was published in 1989, MCAO has been applied commonly to the rat, and often paired with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining for stroke volume measurement. Meanwhile, advances in the ability to genetically alter mice have allowed exciting lines of research into ischemia. Because of technical demands and issues with survival, relatively few laboratories have investigated the MCAO method in the mouse. Our present work utilizes a mouse middle cerebral occlusion (MCAO) model of embolic stroke to study neuronal degeneration following temporary focal cerebral ischemia. C57Bl/6J mice were used to examine the exact effects of MCAO using Fluoro-Jade, a marker of neurodegeneration that allows observation of specific brain regions and cells destined to die. A time course of escalating neuronal degeneration from 10 min to 7 days following MCAO was established. Technical aspects of this popular method for transient focal ischemia as it applies to the mouse are discussed.

Animals↗
PubMed2003

Quantitative analysis of perinatal rodent oligodendrocyte lineage progression and its correlation with human.

The development of a rodent model in the perinatal rat or mouse that reproduces the principal features of human perinatal white matter injury (periventricular leukomalacia) has been hampered by uncertainty about the developmental window in the rodent that coincides temporally with cerebral white matter development in the premature infant. We recently determined oligodendrocyte (OL) lineage progression in human cerebral white matter and found that the late OL progenitor (preOL) predominates throughout the high-risk period for periventricular leukomalacia [J. Neurosci. 21(2001), 1302-1312]. Here, we determined in the perinatal rat and mouse when each species displays a distribution of OL stages that is similar to the premature human cerebral white matter. PreOLs are abundant in the rat and mouse at P2. By P7, extensive OL maturation occurs in both species and coincides with the onset of early myelination. PreOLs and immature OLs mature in the P2 white matter along a medial to lateral gradient. This may provide an explanation for regional variation in the susceptibility of perinatal white matter to injury. We propose that the sequence of OL lineage progression is a useful means to estimate developmental windows of white matter maturation in perinatal rodents that coincide with those of developing human cerebral white matter. These studies support that the vulnerable period for white matter injury in the rodent is centered around P2 and should decline thereafter, coincident with the onset of myelination.

Animals↗
PubMed2001

Gene targeting in the rodent malaria parasite Plasmodium yoelii.

It is anticipated that the sequencing of Plasmodium falciparum genome will soon be completed. Rodent models of malaria infection and stable transformation systems provide powerful means of using this information to study gene function in vivo. To date, gene targeting has only been developed for one rodent malaria species, Plasmodium berghei. Another rodent species, Plasmodium yoelii, however, is favored to study the mechanisms of protective immunity to the pre-erythrocytic stages of infection and vaccine development. In addition, it offers the opportunity to investigate unique aspects of pathogenesis of blood stage infection. Here, we report on the stable transfection and gene targeting of P. yoelii. Purified late blood stage schizonts were used as targets for electroporation with a plasmid that contains a pyrimethamine-resistant form of the P. berghei dihydrofolate reductase-thymidylate synthase (Pbdhfr-ts) fused to green fluorescent protein (gfp) gene. After drug selection, fluorescent parasites contained intact, non-rearranged plasmids that remain stable under drug-pressure. In addition, we used another dhfr-ts/gfp based plasmid to disrupt the P. yoelii trap (thrombospondin-related anonymous protein) locus by site-specific integration. The phenotype of P. yoelii TRAP knockout was identical to that previously reported for the P. berghei TRAP knockout. In the absence of TRAP, the erythrocytic cycle, gametocyte and oocyst development of the mutant parasites were indistinguishable from wild type (WT). Although the sporozoites appeared morphologically normal, they failed to glide and to invade the salivary glands of mosquitoes.

Animals↗
PubMedDate not supplied

Animal models of breast cancer: experimental design and their use in nutrition and psychosocial research.

This is the second Special Issue addressing the diversity and use of animal models of breast cancer. The previous issue (Breast Cancer Res Treat 39:1-135, 1996), dealt with a variety of topics such as the characteristics of chemically- and virally-induced rodent models, immunobiologies of immunedeficient mice, transgenic mouse models, and models of metastasis. In the first part of this second Special Issue, the articles address animal models for studying life-style factors, including psychosocial, exercise, and nutritional research in breast cancer. In the second section, there is emphasis on the controversial area of dietary fat, with other authors addressing caloric restriction and dietary isoflavonoids, retinoids, and monoterpenes in the third part. In the final section, a series of authors provide suggestions for approaching various issues involving experimental design, including nutritional studies, drug screening models, statistical considerations, quantitation of tumor growth kinetics, and animal husbandry. These articles, and some additional issues raised during the previous Special Issue, are briefly discussed in this overview. They include a further evaluation of the relative merits of 7,12-dimethylbenz(a)anthracene and N-nitroso-N-methylurea as carcinogens, and of the use of the AIN76 and AIN93 semipurified diets in studies of mammary carcinogenesis.

Animals↗
PubMed2001

Novel animal models of affective disorders.

Is there an appropriate animal model for human affective disorders? The traditional difficulties in accepting animal models for psychopathology stem from the argument that there is no evidence for concluding that what occurs in the brain of the animal is equivalent to what occurs in the brain of a human. However, if one models any or some core aspects of affective disorder, this model can become an invaluable tool in the analysis of the multitude of causes, genetic, environmental, or pharmacological, that can bring about symptoms homologous to those of patients with affective disorders. Animal models can also allow the study of the mechanisms of specific behaviors, their pathophysiology, and can aid in developing and predicting therapeutic responses to pharmacologic agents. Although animals exhibit complex and varied social and emotional behaviors for which well-validated and standardized measures exist, an understanding that a precise replica of human affective disorders cannot be expected in a single animal model is crucial. Instead, a good animal model of a human disorder should fulfill as many of the four main criteria as possible: (1) strong behavioral similarities, (2) common cause, (3) similar pathophysiology, and (4) common treatment. An animal model fulfilling any or most of these criteria can be used to elucidate the mechanisms of the specific aspect of the model that is homologous to the human disorder. A wide range of animal models of affective disorders, primarily depression, has been developed to date. They include models in which "depressive behavior" is the result of genetic selection or manipulation, environmental stressors during development or in adulthood, or pharmacologic treatments. The assessment of these animal models is based either on behavioral tests measuring traits that are homologous to symptoms of the human disorder they model, or behavioral tests responsive to appropriate pharmacologic treatments. The goal of this review is to focus on relatively recent developments of selected models, to aid in understanding their strengths and weaknesses, and to help those choosing the difficult task of developing novel animal models of affective disorders. The ideal animal model of affective disorders of the future would be an endogenous, genetic model that reiterates the essential, core aspects of the human disease and responds to the standard regimens of therapy. Because complex diseases have been approached from the genetic startpoint by using rodent models, a genetic model of affective disorder would open up possibilities for genetic analysis of polygenic traits that seem to underlie these disorders.

Animals↗
PubMed2006

Understanding our drugs and our diseases.

Analysis of mouse genetic models of human disease-associated traits has provided important insight into the pathogenesis of human disease. As one example, analysis of a murine genetic model of osteoporosis demonstrated that genetic variation within the 15-lipoxygenase (Alox15) gene affected peak bone mass, and that treatment with inhibitors of this enzyme improved bone mass and quality in rodent models. However, the method that has been used to analyze mouse genetic models is very time consuming, inefficient, and costly. To overcome these limitations, a computational method for analysis of mouse genetic models was developed that markedly accelerates the pace of genetic discovery. It was used to identify a genetic factor affecting the rate of metabolism of warfarin, an anticoagulant that is commonly used to treat clotting disorders. Computational analysis of a murine genetic model of narcotic drug withdrawal suggested a potential new approach for treatment of narcotic drug addiction. Thus, the results derived from computational mouse genetic analysis can suggest new treatment strategies, and can provide new information about currently available medicines.

Animals↗
PubMed1991

Medium-term protocols for in vivo evaluation of chemical modifiers of carcinogenesis.

Cancer development is a long-term multistep process which allows interventional measure before the clinical disease emerges. The detection of natural substances which can block the process of carcinogenesis is as important as the identification of anti-tumoral drugs since they might be used in chemoprevention of cancer in high-risk groups. In vivo rodent models of chemical carcinogenesis have been used to study plant-derived inhibitors of carcinogenesis such as indoles, coumarins, isothiocyanates, flavones, phenols and allyl-sulfides. Since the standard in vivo rodent bioassay is prolonged and expensive, shorter reliable protocols are needed. Two in vivo medium-term protocols for evaluation of modifiers of carcinogenesis are presented, one related to liver and the other to bladder cancer. Both protocols use rats, last 8 and 36 weeks and are based on the two-step concept of carcinogenesis: initiation and promotion. The protocols use respectively the development of altered foci of hepatocytes expressing immunohistochemically the placental form of glutathione S-transferase and the appearance of pre-neoplastic urothelium and papillomas as the "end-points". The use of these protocols for detection of plant-derived inhibitors of carcinogenesis appear warranted.

Animals↗
PubMed2003

Experimental models of inflammatory bowel disease.

The etiology and pathogenesis of inflammatory bowel disease (IBD) remains unsolved, but improved experimental models of enterocolitis have led to progress. Intestinal inflammation and experimental IBD can be induced by chemical or dietary factors or by microbial products. Many animal models of IBD can be used to evaluate new anti-inflammatory drugs. These models, however, usually demonstrate acute, self-limiting colitis. The spontaneous colitis models developed in the cotton-top tamarin monkey and the C3H/HeJBir mouse mimic more features of human IBD. Inflammation is chronic and is under genetic control. The differential genetic susceptibility of inbred rat strains to chronic inflammation have been exploited. Lewis rats injected with bacterial products, peptidoglycan polysaccharide or indomethicin develop chronic relapsing enterocolitis, whereas closely related Buffalo or Fisher rat strains develop only transient inflammation. These models are also useful to test the specific inhibition of inflammatory mediators and target molecules. Over-expression (transgenic) or deletion (knockout) of specific genes have led to the development of rodent models of spontaneous colitis. Inflammation arises from a number of mutations of immunomodulatory molecules, supporting the concept of genetic heterogeneity for IBD. The results obtained from experimental models have generated new hypotheses, expanded human studies, and suggested novel forms of therapy for IBD patients.

Animals↗
PubMedDate not supplied

[Urgent problems of experimental modelling of thermal skin burns].

The review presents a critical analysis of principal benefits and shortcomings of standard experimental models of surface and deep thermal burns of the skin. Comparison of the results of experimental studies must rest on reproduction of identical traumas in series of experiments. It is important to choose animals species, burn model, exposition time and thermal agent depending on the study aim. An algorithm of simple and available methods of reproduction of superficial and deep thermal burns of the skin on a rodent model is described.

Animals↗
PubMed2006

Increased depressive-like traits in an animal model of premenstrual irritability.

Women are at higher risk of anxiety and mood disorders, especially at transitions across the reproductive life cycle (premenstruum, postpartum, menopause). Premenstrual dysphoric disorder (PMDD) is one of female mood disorders associated with changing ovarian hormone levels. Because anxiety and depression frequently occur in women with PMDD, premenstrual dysphoria might be a manifestation of certain vulnerability traits increasing the risk of those disorders. The present study was conducted to elucidate a potential association between estrous cycle-dependent aggression, the rodent model of "premenstrual irritability" (resident-intruder test), and anxiety (elevated plus maze), depressive-like traits (forced swim test) as well as carbohydrate craving in female Wistar rats. Some aggressive and nonaggressive females were restraint-stressed before testing to determine their sensitivity to stress at different hormonal stages. The results revealed that females expressing the estrous cycle-dependent aggression but not those not expressing cycle-dependent aggression spent longer time immobile and shorter time swimming in the forced swim test at metestrus compared to proestrus phase of the estrous cycle. There was no difference between aggressive and nonaggressive females in anxiety, locomotor activity and sensitivity to restraint stress and sucrose consumption. The present study suggests a common neurobiological background for the estrous cycle-dependent aggression and depressive-like traits in rodents. This phenomenon could potentially aid the elucidation of premenstrual emotional dysfunctions and might be used as an ethological model to study a biochemical and genetic proneness to depression.

Aggression↗
PubMed1993

44-kd oncofetal transplantation antigen in rodent and human fetal cells. Implications of recrudescence in human and rodent cancers.

OBJECTIVE: This article summarizes the phase-specific nature of a cell surface, 44-kd tumor-associated transplantation antigen glycoprotein expressed during early and middle gestation in a portion of rodent and human fetal cells during normal fetal tissue development and illustrates how this glycoprotein is consistently recrudesced in primary and established human squamous cell carcinomas and other human and rodent tumors. The oncofetal antigen was not detectable in any human or rodent term fetal tissue or normal adult tissues tested. The tumor-associated transplantation antigen was tumor specific, yet not germ-line specific (expressed in lymphomas, sarcomas, and carcinomas) in human or rodent cancers. Rodent model tumor studies have shown 44-kd oncofetal antigen can act as a tumor-associated autoantigen of potential use in cancer detection and therapy. DESIGN: The oncofetal antigen was detected by immunogenicity, flow cytometry, and Western blotting in syngeneic rodent tumor recipients and by the last two methods in humans with progressive cancer. Syngeneically derived mouse monoclonal antibody (MoAb 115) was used to identify 44-kd oncofetal antigen. Early to middle gestation, oncofetal antigen-positive, mouse embryo/fetal cells used to stimulate the hybridoma were tested for immunogenicity as a tumor-associated transplantation antigen in syngeneic hosts. SETTING AND PATIENTS: Patients presenting with head and neck squamous cell carcinoma (N = 25) and other carcinomas at the University of South Alabama Medical Center, Mobile, underwent a biopsy, and the tumors were mechanically dispersed and were then tested for oncofetal antigen expression directly in flow cytometry. The tumors were also cultured and tested as squamous carcinoma cell lines. Growing squamous carcinoma cells and uncultured tumor cells were stained with MoAb 115 or control MoAb. Extracts of the cells were banded by electrophoresis in gels, Western blotted, and reacted with MoAbs and enzyme-linked immunosorbent assay second antibody. Time-mated mouse fetus and human fetal cells were also stained with MoAb 115 or control antibody and analyzed in the flow cytometer. RESULTS: Eight- to 13-day mouse fetal cells conferred protection against syngeneic tumor challenge. Term 18- to 21-day fetal or neonate or adult mouse cells were nonprotective. All head and neck squamous cell carcinomas tested expressed 44-kd oncofetal antigen by flow cytometric analysis and in Western blots as did ATCC cell lines of these tumors, whereas normal control tissues were negative. Second trimester human fetal cells were 44-kd oncofetal antigen positive. A large spectrum of rodent sarcomas and lymphomas express the OFA. CONCLUSIONS: Shared 44-kd oncofetal antigen OFA offers promise as a tumor detection marker in human squamous cell carcinoma and other human carcinoma development, and syngeneic mouse tumors are good model systems to explore oncofetal antigen antigenicity.

Animals↗
PubMed2005

Mast cells are required for optimal autoreactive T cell responses in a murine model of multiple sclerosis.

Once considered to be of sole importance in allergy and parasitic infections, the role of mast cells in other pathologic and protective immune responses is becoming increasingly evident. We previously demonstrated that mast cells contribute to the severity of EAE, the rodent model of multiple sclerosis. Here we show that one mode of mast cell action is through effects on the autoreactive T cell response. Early indices of both peripheral CD4 and CD8 T cell activation, including IFN-gamma production and increases in CD44 and CD11a expression, are attenuated in mast cell-deficient (W/Wv) mice after myelin oligodendrocyte glycoprotein(35-55) priming when compared to WT animals. Reduced infiltrates of activated T cells in the central nervous system are also observed. Importantly, selective repletion of the mast cell compartment restores most T cell responses in the lymph nodes and the central nervous system, correlating with reconstitution of severe disease. The adoptive transfer of WT-derived encephalitogenic T cells results in significantly less severe disease in W/Wv recipients, indicating that mast cells also exert potent effects after the initial T cell response is generated. Our data provide the first in vivo evidence that mast cells can significantly influence T cell responses and suggest that mast cells exacerbate disease during both the inductive and effector phases.

Animals↗