846 resultados para RODENTS
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In connection with parasitological studies carried on during 1949 for the U.S. Public Health Service, the writer collected a considerable number of mammals from the northern edge of the "Endicott" section of the Brooks Range, in Arctic Alaska. The mammalian fauna of this region is poorly known, since apparently no previous collecting has been done here. About 200 microtine rodents were collected, mostly near Tolugak Lake (latitude 68° 24' N, longitude 151° 26' W), near the head of the Anaktuvuk River Valley. A few specimens were also taken at Umiat, on the Colville River, about 80 miles north of Tolugak Lake (latitude 69° 23' N, longitude 152° 10' W). Five species are represented: Clethrionomys rutilis dawsoni (Merriam), Microtus oeconomus macfarlani Merriam, Microtus miurus paneaki, n. subsp., Lemmus trimucronatus alascensis Merriam and Dicrostonyx groenlandicus rubricatus (Richardson). More complete details concerning their ecology and reproduction will be presented in a later paper, at which time the other mammals obtained will also be considered. The specimens have been deposited in the U.S. National Museum.
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Paranoplocephala etholeni n. sp, parasitizing the meadow vole Microtus pennsylvanicus in Alaska and Wisconsin, USA. is described Paranaplocephala etholeni is morphologically most closely related to the Nearctic Paranoplocephala ondatrae (Rausch, 1948). Available data suggest that P. etholeni is a host-specific, locally rare species that may have a wide but sporadic geographical distribution in North America. The finding of P. ondatrae-like cestodes in Microtus spp. suggests that this poorly known species may actually be a parasite of voles rather than muskrat (type host). A tabular synopsis of all the known species of Paranoplocephala s. I. in the Holarctic region with their main morphological features is presented.
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ABSTRACT: Preliminary studies completed on commensal rodents with the new anticoagulant rodenticide difethialone showed very good efficacy, such that 25 ppm baits could be used effectively. New test results presented in this publication confirm the activity as shown under laboratory conditions in choice tests, which represent more severe conditions, as well as its effectiveness against rodents that are resistant and non-resistant to warfarin. In tests where the palatability was only fair the chemical activity resulted in excellent mortality. In a field test against a large population of Mus musculus the results proved very satisfactory. Difethialone is toxic to birds and fish. However, it seems to be better tolerated by dogs and pigs, animals that are frequently on the list of accidental poisonings. Difethialone is stored over a prolonged period in the liver but the risk to non-target species consuming rodents having ingested the compound does not seem to be high. For reasons attributed to the mode of action, difethialone must be handled with precautions as other anticoagulants for which Vitamin Kj is the antidote. In the event of an accidental poisoning, an antidotal therapy plan is proposed. The lower levels of active ingredient in finished baits (25 ppm) should pose a low risk to non-target species.
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The evolution of effective rodent control has been greater in the past 20 years than during the previous 200 years. Mankind need no longer fear the "black death," typhus, and other rodent-borne diseases. Likewise, there is no longer any reason why we must bear the cost of serious economic losses because of commensal rodent damage to property. Unfortunately, the latter still totals many millions of dollars each year. Damage and contamination of food products by house mice now probably equals or exceeds that caused by rats.
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The evolutionary history of Hystricognathi is associated with major transformations in their placental system. Data so far indicate that key characters are independent from size dimensions in medium to very large species. To better understand the situation in smaller species, we analyzed placental development in a spiny rat, Thrichomys laurentinus. Fourteen individuals ranging from early implantation to near term were investigated by histology, immunohistochemistry, proliferation activity and electron microscopy. Placentation in Thrichomys revealed major parallels to the guinea pig and other hystricognath rodents with respect to the early and invasive implantation, the process of trophoblast invasion, the internal organization of the labyrinth and the trophospongium as well as the establishment of the complete inverted yolk sac placenta. In contrast to systematically related small-sized species, the placental regionalization in Thrichomys was characterized by a remarkable lobulated structure and associated growing processes. Reverse to former perspectives, these conditions represented ancient character states of hystricognaths. The subplacenta was temporarily supplied by both the maternal and fetal blood systems, a rare condition among hystricognaths. The extraplacental trophoblast originating from the subplacenta was partly proliferative in mid gestation. In conclusion, the presented results indicated that only minor variations occurred in small-sized hystricognath species, independent of their systematic interrelationships. Previous views were supported that placentation in hystricognaths followed an extraordinary stable pattern, although the group had distinct habitats in South America and Africa that were separated 30-40 million years ago. J. Exp. Zool. (Mol. Dev. Evol.) 318:13-25, 2012. (C) 2011 Wiley Periodicals, Inc.
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This study aimed to develop an equipment and system of resistance exercise (RE), based on squat-type exercise for rodents, with control of training variables. We developed an operant conditioning system composed of sound, light and feeding devices that allowed optimized RE performance by the animal. With this system, it is not necessary to impose fasting or electric shock for the animal to perform the task proposed (muscle contraction). Furthermore, it is possible to perform muscle function tests in vivo within the context of the exercise proposed and control variables such as intensity, volume (sets and repetitions), and exercise session length, rest interval between sets and repetitions, and concentric strength. Based on the experiments conducted, we demonstrated that the model proposed is able to perform more specific control of other RE variables, especially rest interval between sets and repetitions, and encourages the animal to exercise through short-term energy restriction and "disturbing" stimulus that do not promote alterations in body weight. Therefore, despite experimental limitations, we believe that this RE apparatus is closer to the physiological context observed in humans.
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The present work aimed to investigate the effects of acute sucrose treatment on the perception of painful stimuli. Specifically, we sought to determine the involvement of the endogenous opioid peptide-mediated system as well as the role of the mu(1)-opioid receptor in antinociception organisation induced by acute sucrose intake. Nociception was assessed with the tail-flick test in rats (75, 150 and 250 g) of different ages acutely pre-treated with 500 mu L. of a sucrose solution (25, 50, 150 and 250 g/L) or tap water. Young and Adult rats (250 g) showed antinociception after treatment with 50 g/L (during 5 min) and 150 g/L and 250 g/L (during 20 min) sucrose solutions. Surprisingly, this antinociception was more consistent in mature adult rodents than in pups. To evaluate the role of opioid systems, mature adult rodents were pre-treated with different doses (0.25, 1 or 4mg/kg) of the non-selective opioid receptor antagonist naloxone, the selective pi-opioid receptor antagonist naloxonazine or vehicle followed by 250 g/L sucrose solution treatment. Sucrose-induced antinociception was reduced by pre-treatment with both naloxone and naloxonazine. The present findings suggest that sweet substance-induced hypo-analgesia is augmented by increasing sucrose concentrations in young and adult rodents. Acute oral sucrose treatment inhibits pain in laboratory animal by mediating endogenous opioid peptide and mu(1)-opioid receptor actions. (C) 2011 Elsevier Inc. All rights reserved.
Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents
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OBJECTIVES: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life. METHOD: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol. RESULTS: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>7 times), bradycardic responses (>4 times), and vagal (similar to 38%) and sympathetic effects (similar to 36%) were reduced as compared to the control group. CONCLUSION: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance.
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The Akodontini is the second most speciose tribe of sigmodontine rodents, one of the most diverse groups of neotropical mammals. Molecular phylogenetic analyses are discordant regarding the interrelationships of genera, with low support for some clades. However, two clades are concordant, one (clade A) with Akodon sensu strictu (excluding Akodon serrensis), "Akodon" serrensis, Bibimys, Deltamys, Juscelinomys, Necromys, Oxymycterus, Podoxymys, Thalpomys and Thaptomys, and another (clade B) with Blarinomys, Brucepattersonius, Kunsia, Lenoxus and Scapteromys. Here, we present chromosome painting using Akodon paranaensis (APA) Y paint, after suppression of simple repetitive sequences, on ten Akodontini genera. Partial Y chromosome homology, in addition to the homology already reported on the Akodon genus, was detected on the Y chromosomes of "A." serrensis, Thaptomys, Deltamys, Necromys and Thalpomys and on Y and X chromosomes in Oxymycterus. In Blarinomys, Brucepattersonius, Scapteromys and Kunsia, no APA Y signal was observed using different hybridization conditions; APA X paint gave positive signals only on the X chromosome in all genera. The Y chromosome homology was variable in size and positioning among the species studied as follow: (1) whole acrocentric Y chromosome in Akodon and "A." serrensis, (2) Yp and pericentromeric region in submetacentric Y of Necromys and Thaptomys, (3) pericentromeric region in acrocentric Y of Deltamys, (4) distal Yq in the acrocentric Y chromosome of Thalpomys and (5) proximal Yq in the acrocentric Y and Xp in the basal clade A genus Oxymycterus. The results suggest that the homology involves pairing (pseudoautosomal) and additional regions that have undergone rearrangement during divergence. The widespread Y homology represents a phylogenetic signal in Akodontini that provides additional evidence supporting the monophyly of clade A. The findings also raise questions about the evolution of the pseudoautosomal region observed in Oxymycterus. The Y chromosomes of these closely related species seem to have undergone dynamic rearrangements, including restructuring and reduction of homologous segments. Furthermore, the changes observed may indicate progressive attrition of the Y chromosome in more distantly related species.
Cerebral White Matter Oxidation and Nitrosylation in Young Rodents With Kaolin-Induced Hydrocephalus
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Hydrocephalus is associated with reduced blood flow in periventricular white matter. To investigate hypoxic and oxidative damage in the brains of rats with hydrocephalus, kaolin was injected into the cisterna magna of newborn 7- and 21-day-old Sprague-Dawley rats, and ventricle size was assessed by magnetic resonance imaging at 7, 21, and 42 days of age. In-situ evidence of hypoxia in periventricular capillaries and glial cells was shown by pimonidazole hydrochloride binding. Biochemical assay of thiobarbituric acid reaction and immunohistochemical detection of malondialdehyde and 4-hydroxy-2-nonenal indicated the presence of lipid peroxidation in white matter. Biochemical assay of nitrite indicated increased nitric oxide production. Nitrotyrosine immunohistochemistry showed nitrosylated proteins in white matter reactive microglia and astrocytes. Activities of the antioxidant enzymes catalase and glutathione peroxidase were not increased, and altered hypoxia-inducible factor 1 alpha was not detected by quantitative reverse transcription-polymerase chain reaction. Cerebral vascular endothelial growth factor expression determined by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay was not changed, but vascular endothelial growth factor immunoreactivity was increased in reactive astrocytes of hydrocephalic white matter. To determine if nitric oxide synthase is involved in the pathogenesis, we induced hydrocephalus in 7-day-old wild-type and neuronal nitric oxide synthase-deficient mice. At 7 days, the wild-type and mutant mice exhibited equally severe ventriculomegaly and no behavioral differences, although increased glial fibrillary acidic protein was less in the mutant mice. We conclude that hypoxia, via peroxidation and nitrosylation, contributes to brain changes in young rodents with hydrocephalus and that compensatory mechanisms are negligible.
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Toxoplasma gondii is a protozoan parasite that infects humans and other warm-blooded animals; it uses feral and domestic cats as the definitive hosts. Neospora caninum is a protozoan parasite of animals whose life cycle is very similar to T. gondii but uses canids as definitive hosts. Small rodents play an important role in the life cycle of T. gondii, and a few findings indicated that they may be natural intermediate hosts for N. caninum. The present study was aimed at identifying infections by T. gondii and N. caninum in urban rodents. Infections by T. gondii were quantified using isolation of the parasite by bioassay in mice; molecular methods were also used for both parasites. Overall, 217 rodents were captured. Brain and heart tissues of all rodents were bioassayed in mice for the detection of T. gondii infection. Brain and heart tissues of 121 rodents had the DNA extracted for molecular analysis. Toxoplasma gondii was isolated by bioassay from a single rodent. From the 121 rodents tested for the presence of T. gondii DNA, 2 animals were positive. In contrast, DNA of N. caninum was not detected in any of the samples. In conclusion, the surveys of N. caninum and T. gondii infection in Rattus rattus, Rattus norvegicus, and Mus musculus captured in urban areas of Sao Paulo reveal a striking low frequency of occurrence of these infections.
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Abstract Background Because cardiomyopathy is the leading cause of death in diabetic patients, the determination of myocardial function in diabetes mellitus is essential. In the present study, we provide an integrated approach, using noninvasive echocardiography and invasive hemodynamics to assess early changes in myocardial function of diabetic rats. Methods Diabetes was induced by streptozotocin injection (STZ, 50 mg/kg). After 30 days, echocardiography (noninvasive) at rest and invasive left ventricular (LV) cannulation at rest, during and after volume overload, were performed in diabetic (D, N = 7) and control rats (C, N = 7). The Student t test was performed to compare metabolic and echocardiographic differences between groups at 30 days. ANOVA was used to compare LV invasive measurements, followed by the Student-Newman-Keuls test. Differences were considered significant at P < 0.05 for all tests. Results Diabetes impaired LV systolic function expressed by reduced fractional shortening, ejection fraction, and velocity of circumferential fiber shortening compared with that in the control group. The diabetic LV diastolic dysfunction was evidenced by diminished E-waves and increased A-waves and isovolumic relaxation time. The myocardial performance index was greater in diabetic compared with control rats, indicating impairment in diastolic and systolic function. The LV systolic pressure was reduced and the LV end-diastolic pressure was increased at rest in diabetic rats. The volume overload increased LVEDP in both groups, while LVEDP remained increased after volume overload only in diabetic rats. Conclusion These results suggest that STZ-diabetes induces systolic and diastolic dysfunction at rest, and reduces the capacity for cardiac adjustment to volume overload. In addition, it was also demonstrated that rodent echocardiography can be a useful, clinically relevant tool for the study of initial diabetic cardiomyopathy manifestations in asymptomatic patients.
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Rodents are most useful models to study physiological and pathophysiological processes in early development, because they are born in a relatively immature state. However, only few techniques are available to monitor non-invasively heart frequency and respiratory rate in neonatal rodents without restraining or hindering access to the animal. Here we describe experimental procedures that allow monitoring of heart frequency by electrocardiography (ECG) and breathing rate with a piezoelectric transducer (PZT) element without hindering access to the animal. These techniques can be easily installed and are used in the present study in unrestrained awake and anesthetized neonatal C57/Bl6 mice and Wistar rats between postnatal day 0 and 7. In line with previous reports from awake rodents we demonstrate that heart rate in rats and mice increases during the first postnatal week. Respiratory frequency did not differ between both species, but heart rate was significantly higher in mice than in rats. Further our data indicate that urethane, an agent that is widely used for anesthesia, induces a hypoventilation in neonates whilst heart rate remains unaffected at a dose of 1 g per kg body weight. Of note, hypoventilation induced by urethane was not detected in rats at postnatal 0/1. To verify the detected hypoventilation we performed blood gas analyses. We detected a respiratory acidosis reflected by a lower pH and elevated level in CO2 tension (pCO2) in both species upon urethane treatment. Furthermore we found that metabolism of urethane is different in P0/1 mice and rats and between P0/1 and P6/7 in both species. Our findings underline the usefulness of monitoring basic cardio-respiratory parameters in neonates during anesthesia. In addition our study gives information on developmental changes in heart and breathing frequency in newborn mice and rats and the effects of urethane in both species during the first postnatal week.
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Während des frühen Lebens stellen epileptische Anfälle schwere neurologische Zustände dar, weil sie ein großer Risikofaktor für die Manifestation der Epilepsie sind und eine hohe pharmakologische Resistenz zeigen. In meiner Doktorarbeit konzentrierte ich mich auf die Frage, wie verschiedene Neurotransmitter-Systeme und klinisch verwendete Medikamente epileptiforme Entladungen im perinatalen Hippocampus beeinflussen. rnIm ersten Teil meines Projektes untersuchte ich die Wirkung von GABA-Antagonisten und Modulatoren, die zwischen phasischen und tonischen GABAergen Strömen differenzieren, auf Feldpotentialaktivität in Hippocampusschnitten. Diese Experimente zeigten, dass im unreifen Hippocampus synaptische GABAerge Aktivität benötigt wird, um die Erregbarkeit zu begrenzen, während tonische GABAerge Ströme die Erregbarkeit verstärken können. Dies könnte darauf hinweisen, dass Antiepileptika mit einer höheren Spezifität für synaptische GABAA-Rezeptoren wirksamer zur Behandlung von epileptischen Anfällen bei Neugeborenen sein können. rnUm den Einfluss von Dopamin auf die Erregbarkeit des unreifen Hippocampus herauszufinden, untersuchte ich im zweiten Teil meiner Arbeit die Wirkung von verschiedenen Dopaminkonzentrationen und spezifische Agonisten und Antagonisten der Dopamin-Rezeptor-Subtypen auf epileptiforme Entladungen. Diese Experimente zeigten, dass niedrige Dopamin Konzentrationen eine antikonvulsive Wirkung haben, welche vom D2-ähnliche-Rezeptor-Agonisten Quinpirol nachgeahmt werden kann, während höhere Dopamin-Konzentrationen eine prokonvulsive Wirkung über Aktivierung von D1-ähnlichen Rezeptoren hervorrufen. Obwohl unsere Untersuchungen eine mögliche Verwendung von D2-ähnlichen Rezeptor-Agonisten zur Kontrolle epileptischer Anfälle in Neugeborenen nahelegen, müssen mögliche negative Auswirkungen von DAergen Agonisten und Antagonisten auf die neuronale Entwicklung berücksichtigt werden.rnIm dritten Teil meiner Arbeit untersuchte ich welche Konzentrationen von Methylxanthinen epileptische Anfälle in Hippocampuspreparationen auslösen die synaptische Übertragungen verändern können. Diese Experimente zeigten, dass sowohl Theophyllin als auch Koffein in höheren Konzentrationen die basale synaptische Übertragungen in der CA1-Region des Hippocampus modifizieren und epileptiforme Entladungen provozieren. Die Auswirkungen auf die postsynaptischen Antworten und spontanen epileptiformen Entladungen durch Koffein waren weniger ausgeprägt, was darauf hindeutet, dass diese Substanz potentiell vorteilhafter für therapeutische Anwendungen bei Frühgeborenen sein kann. rnZusammenfassend bereichern die Ergebnisse meiner Studie erheblich unser Wissen über die zugrunde liegenden Mechanismen epileptiformer Aktivität im unreifen Hippocampus und den therapeutischen Einsatz von Methylxanthinen und Pharmaka, die auf das GABAerge und DArge System einwirken.rnrn
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While incretins are of great interest for the therapy of diabetes 2, the focus has recently been brought to the thyroid, since rodents treated with glucagon-like peptide-1 (GLP-1) analogs were found to occasionally develop medullary thyroid carcinomas. Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. Receptor incidence and density were assessed and compared with the receptor expression in human thyroids, medullary thyroid carcinomas, and TT cells. GLP-1 receptors are expressed in C cells of normal rat and mice thyroids. Their density is markedly increased in rat C-cell hyperplasia and medullary thyroid carcinomas, where their incidence amounts to 100%. GIP receptors are neither detected in normal rodent thyroids nor in C-cell hyperplasia, but are present in all rat medullary thyroid carcinomas. No GLP-1 or GIP receptors are detected in normal human thyroids. Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. TT cells lack GLP-1 receptors but express GIP receptors. GLP-1 receptors are frequently expressed in non-neoplastic and neoplastic C cells in rodents while they are rarely detected in human C-cell neoplasia, suggesting species differences. Conversely, GIP receptors appear to be massively overexpressed in neoplastic C cells in both species. The presence of incretin receptors in thyroid C cell lesions suggests that this organ should be monitored before and during incretin-based therapy of diabetes.