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PubMed2004

End-to-side neurorrhaphies in a rodent model of peripheral nerve injury: a preliminary report of a novel technique.

OBJECT: The standard techniques for repair of peripheral nerve injuries with neuroma formation are typically suboptimal. To begin to explore alternative techniques, the authors used an established model in rodents by using end-to-side "terminolateral" neurorrhaphies (TLNs) to study alternative grafting techniques. The TLN "jump grafts" bypass a neuromain-continuity, hypothetically maintaining functional units within the neuroma to facilitate functional regeneration. Evaluation of the extent and origin of the regenerating fibers within the grafts was also undertaken. METHODS: The right tibial nerve in four adult Sprague-Dawley rats was injured using either a crush or transection technique and compared with four uninjured controls. The contralateral peroneal nerve was immediately harvested for microsurgical repair by using TLN jump grafts in all animals. Following a 3-month recovery, the repaired nerves were evaluated electrophysiologically by using evoked electromyography (EMG). Histological preparation was then performed using dual-fluorescent labeling to study axonal regeneration and origins. Evoked EMG evaluation confirmed healthy electrical conduction across the repair, which was unchanged after transection of the neuroma, but was abolished after transection of the jump graft, indicating functional neural regeneration across both the proximal and distal TLNs of the jump grafts. Fluorescent tracing analysis confirmed regeneration across both the proximal and distal portion of the jump grafts, demonstrated both motor and sensory neurons as the source of the regenerating fibers, and demonstrated significant numbers of double-labeled cell bodies, indicating that collateral sprouting was the primary source of regenerating fibers. CONCLUSIONS: The authors have preliminarily shown that regeneration occurs both electrophysiologically and histologically with a double-TLN jump graft. Clinically, this method could offer an alternative strategy for the technique and timing of neuroma repair.

Animals↗
PubMed2006

Discrimination learning and reversal of the conditioned eyeblink reflex in a rodent model of autism.

Offspring of rats exposed to valproic acid (VPA) on gestational day (GD) 12 have been advocated as a rodent model of autism because they show neuron loss in brainstem nuclei and the cerebellum resembling that seen in human autistic cases . Studies of autistic children have reported alterations in acquisition of classical eyeblink conditioning and in reversal of instrumental discrimination learning . Acquisition of discriminative eyeblink conditioning depends on known brainstem-cerebellar circuitry whereas reversal depends on interactions of this circuitry with the hippocampus and prefrontal cortex. In order to explore behavioral parallels of the VPA rodent model with human autism, the present study exposed pregnant Long-Evans rats to 600 mg/kg VPA on GD12 and tested their offspring from Postnatal Day (PND26-31) on discriminative eyeblink conditioning and reversal. VPA rats showed faster eyeblink conditioning, consistent with studies in autistic children . This suggests that previously reported parallels between human autism and the VPA rodent model with respect to injury to brainstem-cerebellar circuitry are accompanied by behavioral parallels when a conditioning task engaging this circuitry is used. VPA rats also showed impaired reversal learning, but this likely reflected "carry-over" of enhanced conditioning during acquisition rather than a reversal learning deficit like that seen in human autism. Further studies of eyeblink conditioning in human autism and in various animal models may help to identify the etiology of this developmental disorder.

Analysis of Variance↗
PubMed1988

Chronic cyclosporine nephrotoxicity. A rodent model.

The lack of a suitable rodent model has hampered the study of chronic cyclosporine nephrotoxicity. Proximal tubule vacuolization and inclusions are consistently reported in rat studies, but changes associated with chronic CsA nephrotoxicity in humans (interstitial fibrosis, tubular atrophy, arteriolopathy) are difficult to reproduce. Using male Sprague-Dawley (SD) rats we have administered CsA in olive oil (o.o.) at 25 mg/kg/d i.p. for 28 consecutive days. This protocol consistently results in a lesion of patchy interstitial fibrosis, tubular atrophy, interstitial inflammation, and marked juxtaglomerular apparatus (JGA) hypertrophy and hyperplasia. Control animals were pair-fed and received only o.o. i.p. Despite pair feeding, CsA-treated animals gained only 9.4 +/- 12 g, while controls gained 69 +/- 18 g. Minimal JGA hypertrophy was noted in some control animals, but no other significant changes were identified. The protocol was well tolerated and did not result in peritonitis. GFR was significantly depressed in the CsA-treated animals at the end of the 28-day period (0.44 +/- .26 vs. 1.12 +/- .13 ml/min) and BP tended to be lower, but this difference did not achieve statistical significance. We conclude that this model results in a reproducible lesion with many of the features of chronic CsA nephrotoxicity in humans, and that it will permit study of this problem to advance.

Animals↗
PubMed2005

Effects of space flight conditions on the function of the immune system and catecholamine production simulated in a rodent model of hindlimb unloading.

UNLABELLED: The rodent model of hindlimb unloading has been successfully used to simulate some of the effects of space flight conditions. Previous studies have indicated that mice exposed to hindlimb-unloading conditions have decreased resistance to infections compared to restrained and normally housed control mice. OBJECTIVE: The purpose of this study was to clarify the mechanisms involved in resistance to infection in this model by examining the effects of hindlimb unloading on the function of the immune system and its impact on the production of catecholamines. METHODS: Female Swiss Webster mice were hindlimb-unloaded during 48 h and the function of the immune system was assessed in spleen and peritoneal cells immediately after this period. In addition, the kinetics of catecholamine production was measured throughout the hindlimb-unloading period. RESULTS: The function of the immune system was significantly suppressed in the hindlimb-unloaded group compared to restrained and normally housed control mice. Levels of catecholamines were increased in the hindlimb-unloaded group and peaked at 12 h following the commencement of unloading. CONCLUSION: These results suggest that physiological responses of mice are altered early after hindlimb unloading and that catecholamines may play a critical role in the modulation of the immune system. These changes may affect the ability of mice to resist infections.

Animals↗
PubMed1995

Rodent models for the study of etiology, prevention and treatment of breast cancer.

Rodent models have been, and continue to be, important in both defining the etiology of breast cancer, and in generating new prevention and treatment strategies directed at this prevalent malignancy. Of all solid cancers, breast cancer has the widest variety of rodent models. Models in rats and mice include both spontaneous, induced and transplantable carcinomas in standard strains. In addition, many strains are available for modeling inherited susceptibility and resistance to breast cancer. Finally, many new models that have taken advantage of techniques from biotechnology such as transgenic, knock-out and gene therapy technologies are being used to evaluate new prevention and treatment strategies for breast cancer.

Animals↗
PubMed1991

A rodent model of cirrhosis, ascites, and bacterial peritonitis.

We sought to develop a rodent model of spontaneous bacterial peritonitis and report here the preliminary results of carbon tetrachloride-induced cirrhosis in which ascites and bacterial peritonitis predictably develop. Of 41 rats that survived the initial carbon tetrachloride toxicity, 38 (92.7%) developed cirrhosis with ascites. Of these 38, 21 (55.3%) developed 24 episodes of ascitic fluid infection without iatrogenic colonization. No surgically treatable source of infection was identified at autopsy in any rat; therefore, the infections were presumed to be "spontaneous." Eight (50%) of the 16 rats with culture-positive ascitic fluid at postmortem examination also had spontaneous pleural fluid infection with the same organism. Escherichia coli and Proteus sp. were the organisms most commonly isolated. This rodent model of cirrhosis with ascites appears to be the first high-yield animal model of spontaneous bacterial peritonitis. Ascitic fluid infection in these rats resembles ascitic fluid infection in humans. This model will allow further investigation of the mechanisms of pathogenesis of ascitic fluid infection and provide insight into the prevention and treatment of spontaneous bacterial peritonitis and pleural fluid infection in patients with cirrhosis.

Animals↗
PubMed2005

How good are rodent models of carcinogenesis in predicting efficacy in humans? A systematic review and meta-analysis of colon chemoprevention in rats, mice and men.

Tumours in rodent and human colon share many histological and genetic features. To know if rodent models of colon carcinogenesis are good predictors of chemopreventive efficacy in humans, we conducted a meta-analysis of aspirin, beta-carotene, calcium, and wheat bran studies. Controlled intervention studies of adenoma recurrence in human volunteers were compared with chemoprevention studies of carcinogen-induced tumours in rats, and of polyps in Min (Apc(+/-)) mice: 6714 volunteers, 3911 rats and 458 mice were included in the meta-analyses. Difference between models was small since most global relative risks were between 0.76 and 1.00. A closer look showed that carcinogen-induced rat studies matched human trials for aspirin, calcium, carotene, and were compatible for wheat bran. Min mice results were compatible with human results for aspirin, but discordant for calcium and wheat bran (no carotene study). These few results suggest that rodent models roughly predict effect in humans, but the prediction is not accurate for all agents. Based on three cases only, the carcinogen-induced rat model seems better than the Min mouse model. However, rodent studies are useful to screen potential chemopreventive agents, and to study mechanisms of carcinogenesis and chemoprevention.

Animals↗
PubMed2003

Alopecia areata susceptibility in rodent models.

With our current view of alopecia areata as an autoimmune disease, it is probable that disease development in an individual is dependent on multiple genetic and environmental factors interacting in a complex system. Rodent models afford the opportunity to investigate alopecia areata development and to define the significance of the different factors involved. Recently, rodent model characterization has been conducted using flow cytometry, microarray analysis, and functional studies. From these a pattern of events in alopecia areata development has emerged. Although the preliminary activation events for the onset of alopecia areata remain unknown, the response of the immune system is characterized by antigen presentation and costimulation of lymphocytes in the lymph nodes and skin, a deficiency of CD4+/CD25+ regulatory cells, and an action of activated lymphocytes on hair follicles via Fas/FasL signaling and cytokines. Thus, onset of disease may require appropriate (or inappropriate) expression of stimulatory antigens within the hair follicle, the breakdown of the putative hair follicle immune privilege, the presentation of antigens to the immune system, a failure of immune system regulation, and the ability of the activated immune system to disrupt anagen-stage hair follicles. Once the sequence of events is initiated, it may become a self-perpetuating cycle, with epitope spreading leading to a wider range of targets in chronic alopecia areata. Rodent model studies have provided significant insight into alopecia areata, but much more remains to be explained about the mechanisms of disease development.

Alopecia Areata↗
PubMed1997

Cytokine regulation of host defense against parasitic gastrointestinal nematodes: lessons from studies with rodent models.

Studies with rodents infected with Trichinella spiralis, Heligmosomoides polygyrus, Nippostronglyus brasiliensis, and Trichuris muris have provided considerable information about immune mechanisms that protect against parasitic gastrointestinal nematodes. Four generalizations can be made: 1. CD4+ T cells are critical for host protection; 2. IL-12 and IFN-gamma inhibit protective immunity; 3. IL-4 can: (a) be required for host protection, (b) limit severity of infection, or (c) induce redundant protective mechanisms; and 4. Some cytokines that are stereotypically produced in response to gastrointestinal nematode infections fail to enhance host protection against some of the parasites that elicit their production. Host protection is redundant at two levels: 1. IL-4 has multiple effects on the immune system and on gut physiology (discussed in this review), more than one of which may protect against a particular parasite; and 2. IL-4 is often only one of multiple stimuli that can induce protection. Hosts may have evolved the ability to recognize features that characterize parasitic gastrointestinal nematodes as a class as triggers for a stereotypic cytokine response, but not the ability to distinguish features of individual parasites as stimuli for more specific protective cytokine responses. As a result, hosts deploy a set of defense mechanisms against these parasites that together control infection by most members of that class, even though a specific defense mechanism may not be required to defend against a particular parasite and may even damage a host infected with that parasite.

Animals↗
PubMed1991

Immunomodulation in the treatment of endometriosis-associated subfertility: use of pentoxifylline to reverse the inhibition of fertilization by surgically induced endometriosis in a rodent model.

OBJECTIVE: To determine the effect of pentoxifylline on early reproductive performance in an animal model for endometriosis. DESIGN: Preclinical blinded study in a rodent model. SETTING: Animal research laboratory. PARTICIPANTS: Sexually mature female golden hamsters. INTERVENTIONS: At laparotomy, groups of hamsters were subjected to: (1) excision of the right uterine horn and (2) excision of the right uterine horn with explantation of four 2-cm2 uterine fragments onto the left uterine mesentery. Six weeks later, surgically treated hamsters and nonsurgically treated controls were subjected to ovulation induction with pregnant mare serum gonadotropin and human chorionic gonadotropin; subsequently, hamsters were divided into groups for periovulatory treatment with either pentoxifylline (2.5 mg/kg) or vehicle given subcutaneously every 8 hours. All hamsters were mated with proven males and killed after 48 hours. MAIN OUTCOME MEASURES: Numbers of unfertilized oocytes and embryos recovered from the left uterine horn at 48 hours after mating. RESULTS: Fertilization rates in surgical and nonsurgical control groups exceeded 90%. Fertilization was significantly impaired in saline-treated animals bearing uterine explants (mean of 2.3% +/- 1.9%). Administration of pentoxifylline dramatically reversed this effect (99.0% +/- 0.7% mean fertilization rate). CONCLUSION: These data suggest that periovulatory treatment with pentoxifylline abrogated the adverse influence of endometrial explants on fertilization in the rodent model. Periovulatory administration of nonteratogenic immunomodulatory agents may provide an alternative to conventional treatment for endometriosis.

Adjuvants, Immunologic↗
PubMed1999

United States-Japan workshop on New Rodent Models for the Analysis and Prevention of Carcinogenesis.

In assessing the present status of rodent models for the analysis and prevention of carcinogenesis, the discussion emphasized that models exist for very few of the major cancers occurring in the United States and Japan. Almost without exception, those that do exist were invented for etiological and mechanistic studies of chemical and physical carcinogenesis. Applicability to cancer chemoprevention was not a primary objective in their development. However, they have been adapted and used for identifying and characterizing chemopreventive agents out of necessity. It is therefore not surprising that they generally fail to fulfill most or all of the requisites of "ideal" models enumerated above, and consequently, the validity of data produced through their use has been questioned. Evolution of future mechanistic models may similarly lead to their eventual adaptation to chemoprevention, but advances will be fragmentary, and the rate of progress seems likely to be slow. Animal models discussed at this workshop were designed specifically for this purpose and promise to expedite the accumulation of valuable new information. Nonetheless, recurrent discussion identified the urgent need for institution of a major, dedicated research initiative with the expressed objective of developing rodent models for organ-specific chemoprevention based on current understanding of underlying genetic and cellular processes. No concerted programs with this objective presently exist either in the United States or Japan. In addition to research specifically designed to meet this need, efforts should be made to involve investigators developing mechanistic animal models in the validation of their models through modulating cancer development by chemopreventive agents. Support for such research initiatives will be essential to continued progress toward the overall objective of identifying safe and effective cancer chemopreventive agents.

Animals↗
PubMed1980

Does the rodent model adequately predict the effects of ozone induced changes to human erythrocytes?

There is an important need to develop animal models to simulate the response of humans to environmental pollutants. The rodent model has been commonly employed to predict the effects of ambient ozone on human RBCs. The use of rodent models for such a purpose is questioned. This challenge is based on the a) ability of mice to significantly enhance ascorbic acid synthesis following ozone stress, b) the ability of ascorbic acid to prevent oxidant [i.e. acetylphenylhydrazine (APH)] stress to human G-6-PD deficient RBCs and c) the lack of ability of humans to synthesize ascorbic acid.

Animals↗
PubMedDate not supplied

Rodent models of nephropathy associated with type II diabetes.

End-stage renal disease from diabetic nephropathy, mainly due to type II diabetes, is an increasing problem in Western countries. The pathogenesis of diabetic nephropathy is still incompletely understood and much of the experimental insight has been obtained from insulinopenic animal models, resembling type I diabetes. This review therefore aims to describe available rodent models of nephropathy associated with type II diabetes. The review focusses on the metabolic as well as renal functional and structural changes. The usefulness of these rodent models to study renal involvement in type II diabetes is discussed with particular emphasis on confounding factors such as hyperlipidemia, hypertension, immunologic abnormalities, urogenital structural abnormalities and other associated pathological conditions. In addition recent observations on two rat strains, the obese Zucker (fatty) and Goto Kakizaki (GK) rat, are discussed in detail.

Animals↗
PubMed2005

Rodent models of focal stroke: size, mechanism, and purpose.

Rodent stroke models provide the experimental backbone for the in vivo determination of the mechanisms of cell death and neural repair, and for the initial testing of neuroprotective compounds. Less than 10 rodent models of focal stroke are routinely used in experimental study. These vary widely in their ability to model the human disease, and in their application to the study of cell death or neural repair. Many rodent focal stroke models produce large infarcts that more closely resemble malignant and fatal human infarction than the average sized human stroke. This review focuses on the mechanisms of ischemic damage in rat and mouse stroke models, the relative size of stroke generated in each model, and the purpose with which focal stroke models are applied to the study of ischemic cell death and to neural repair after stroke.

Animals↗
PubMed1998

Evidence for a unique profile of levetiracetam in rodent models of seizures and epilepsy.

The protective and adverse effect potentials of levetiracetam ((S)-alpha-ethyl-2-oxo-pyrrolidine acetamide) in rodent models of seizures and epilepsy were compared with the profile of several currently prescribed and newly developed antiepileptic drugs. Levetiracetam was devoid of anticonvulsant activity in the acute maximal electroshock seizure test and in the maximal pentylenetetrazol seizure test in mice (up to 540 mg/kg, i.p.) but exhibited potent protection against generalised epileptic seizures in electrically and pentylenetetrazol-kindled mice (ED50 values = 7 and 36 mg/kg, respectively, i.p.). This differs markedly from established and most new antiepileptic drugs which induce significant protection in both the acute seizure tests and the kindling models. Furthermore, levetiracetam was devoid of anticonvulsant activity in several maximal chemoconvulsive seizure tests although an interesting exception was the potent protection observed against secondarily generalised activity from focal seizures induced by pilocarpine in mice (ED50 value = 7 mg/kg, i.p.), pilocarpine and kainic acid in rats (minimum active dose = 17 and 54 mg/kg, respectively, i.p.). The protection afforded by levetiracetam on the threshold for methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM)-induced seizures persisted after chronic administration (17-170 mg/kg, i.p., twice daily/14 days) and levetiracetam did not lower the seizure threshold for the proconvulsant action of the inverse benzodiazepine receptor agonist, N-methyl-beta-carboline-3-carboxamide (FG 7142). The main metabolite of levetiracetam (ucb L057; (S)-alpha-ethyl-2-oxo-1-pyrrolidine acetic acid) was found to be inactive in sound-sensitive mice after acute administration of doses up to 548 mg/kg, i.p. Levetiracetam induced only minor behavioural alterations in both normal and amygdala-kindled rats (54-1700 mg/kg, i.p.) resulting in an unusually high safety margin between rotarod impairment and seizure suppression of 148 in corneally kindled mice and 235 in Genetic Absence Epilepsy Rats from Strasbourg. In comparison, existing antiepileptic drugs have ratios between 2 and 17 in the corneally kindled mouse model. These studies reveal a unique profile of levetiracetam in rodent models. Characteristics are a general lack of anticonvulsant activity against maximal, acute seizures and selective protection with a very high safety margin in genetic and kindled animals and against chemoconvulsants producing partial epileptic seizures. This activity differs markedly from that of the established and newly introduced antiepileptic drugs and appears to derive from the parent compound since its major metabolite was inactive in all models studied. Together these results therefore suggest that levetiracetam may offer an effective, broad-spectrum treatment of epileptic seizures in patients, with a minimum of adverse effects.

Amygdala↗
PubMed2006

mGlu1 and mGlu5 receptor antagonists lack anticonvulsant efficacy in rodent models of difficult-to-treat partial epilepsy.

Modulation of metabotropic glutamate (mGlu) receptors represents an interesting new approach for the treatment of a range of neurological and psychiatric disorders. Several lines of evidence suggest that functional blockade of group I (mGlu1 and mGlu5) receptors may be beneficial for treatment of epileptic seizures. This study was conducted to investigate whether mGlu1 or mGlu5 receptor antagonists have the potential to block partial or secondarily generalized seizures as occurring in partial epilepsy, the most common and difficult-to-treat type of epilepsy in patients. For this purpose, we systemically administered novel highly selective and brain penetrable group I mGlu receptor antagonists, i.e., the mGlu1 receptor antagonist EMQMCM [3-ethyl-2-methyl-quinolin-6-yl-(4-methoxy-cyclohexyl)-methanone methanesulfonate] and the mGlu5 receptor antagonist MTEP ([(2-methyl-1,3-thiazol-4-yl) ethynyl] pyridine), at doses appropriate for mGlu1 or mGlu5 receptor-mediated effects in rodent models of partial seizures. Two models were used: the 6-Hz electroshock model of partial seizures in mice and the amygdala-kindling model in rats. Clinically established antiepileptic drugs were included in the experiments for comparison. Antiepileptic drugs exerted significant anticonvulsant effects in both models, while EMQMCM and MTEP were ineffective in this regard, although both compounds were administered up to doses associated with essentially full receptor occupancy and with typical mGlu receptor-mediated effects in rodent models of anxiety or pain. Brain microdialysis for determining extracellular levels of MTEP following i.p. administration in rats substantiated that effective brain concentrations were reached at times of our experiments in seizure models. The present results do not support a significant anticonvulsant potential of group I mGlu receptor antagonists in rodent models of difficult-to-treat partial epilepsy.

Animals↗
PubMed2004

Metaiodobenzylguanidine and hyperglycemia augment tumor response to isolated limb perfusion in a rodent model of human melanoma.

BACKGROUND: Perfusate acidification with dilute hydrochloric acid augments tumor response rates in a rodent model of isolated limb perfusion (ILP). This study investigates the combination of metaiodobenzylguanidine (MIBG), a mitochondrial inhibitor, and systemic hyperglycemia as a strategy to selectively acidify tumors and thereby sensitize them to ILP. METHODS: Human melanoma xenografts were implanted into the hind limbs of athymic rats. When tumors reached 12 to 15 mm in diameter, animals were randomized to ILP with or without melphalan, with or without systemic MIBG, and hyperglycemia of 485 +/- 35 mg/dL. Intratumoral pH was measured during MIBG and glucose treatment by using magnetic resonance spectroscopy. RESULTS: MIBG at 30 mg/kg plus hyperglycemia decreased intracellular pH by.6 units and extracellular pH by.8 units. MIBG at 22.5 mg/kg plus hyperglycemia decreased intracellular and extracellular pH by.4 and.5 units, respectively. Tumor growth was unaffected by systemic MIBG and hyperglycemia alone. When MIBG at 30 mg/kg and hyperglycemia were combined with ILP, tumor growth was delayed for 33 days after control ILP and for 44 days after melphalan ILP. However, this dose of MIBG was complicated by a 40% mortality rate after ILP. MIBG at 22.5 mg/kg, in combination with MIBG in the perfusate, did not cause mortality and delayed tumor growth by 51 days after melphalan ILP. CONCLUSIONS: MIBG and hyperglycemia improve tumor response rates after ILP in a rodent model of human melanoma. Selective tumor acidification with MIBG and hyperglycemia may offer added benefit to current regional perfusion strategies.

3-Iodobenzylguanidine↗
PubMed2001

Skeletal muscle ischaemia-reperfusion injury: further characterisation of a rodent model.

BACKGROUND: Postischaemic damage in skeletal muscle may be reflected in changes to microvascular blood flow, vascular permeability, and subsequent tissue viability. Previous preclinical studies have not addressed all these parameters, and have not used periods of ischaemia and reperfusion relevant to the clinical setting. This study aimed to develop an animal model hindlimb ischaemia-reperfusion to simulate acute lower limb ischaemia. METHODS: A rodent model of hindlimb tourniquet-induced ischaemia-reperfusion was employed. Gastrocnemius muscle blood flow (GMBF; radio-labelled microspheres), oedema (GMO; using a wet:dry ratio method) and viability (GMV; histochemistry and computerised planimetry) were quantified. RESULTS: 6 h ischaemia per seresulted in neither muscle oedema nor loss of viability, but these changes were apparent following 4 h reperfusion. Early reperfusion at 10 min demonstrated low reflow, with GMBF improving at 120 min before declining sharply at 240 min. CONCLUSION: Prolonged hindlimb ischaemia followed by reperfusion in this rodent model caused significant reductions in gastrocnemius muscle blood flow, associated with muscle oedema and necrosis. These three parameters have not been previously reported together in the same model. This reproducible model could be used in the evaluation of potential therapeutic intervention strategies aimed at ameliorating skeletal muscle reperfusion injury.

Animals↗