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PubMed1992

A correlative study of calcium channel antagonist binding and local neuropathological features in the hippocampus in Alzheimer's disease.

[3H]PN200-110 binding sites were studied by means of quantitative autoradiography in hippocampal sections of patients with Alzheimer's disease and age-matched control subjects. Choline acetyltransferase activity, plaque, tangle and cell densities were also determined in the same tissue samples used for autoradiographic studies. Quantitative autoradiographic analysis of [3H]PN200-110 binding in control hippocampus revealed a heterogeneous pattern similar to that described in rodents, being particularly high in the dentate gyrus. In Alzheimer's disease, [3H]PN200-110 binding was markedly reduced in the subiculum (control = 9.85 +/- 1.41 pmol/g; Alzheimer = 3.41 +/- 0.54 pmol/g, mean +/- S.E.M., P less than 0.001). In the subiculum there was a disproportionate reduction of [3H]PN200-110 binding in comparison to cell loss in Alzheimer's disease. The activity of choline acetyltransferase in the hippocampus was markedly reduced in Alzheimer's disease (controls 6.9 +/- 1.0; Alzheimer 2.7 +/- 0.9 nmol/h/mg protein, mean +/- S.E.M., P less than 0.01). There was a strong correlation between choline acetyltransferase activity and [3H]PN200-110 binding in the subiculum. [3H]PN200-110 binding did not correlate with plaque density in the subiculum. The discrete reduction and preservation of [3H]PN200-110 binding in the present study is consistent with the pattern of selective cellular vulnerability in the hippocampal region in Alzheimer's disease.

Aged↗

PubMed2005

Lack of acute cardioprotective effect from preischaemic erythropoietin administration in a porcine coronary occlusion model.

BACKGROUND: Recombinant human erythropoietin (rhEPO) has been proposed to possess important tissue protective, apart from haematopoietic, effects. Cardioprotective effects have thus been reported in rodents exposed to myocardial ischaemia. Pathways common to the mediation of ischaemic preconditioning may be involved. Before clinical testing such possible cardioprotective effects needs assessment in an experimental large animal model with closer similarity to human ischaemic pathophysiology. METHODS: A control group and two rhEPO groups were studied. EPO1 pigs were given EPO corresponding to the early window and EPO2 pigs to the early and late window of ischaemic preconditioning in a closed chest, catheter-based, porcine coronary occlusion model (45 min of occlusion of the left anterior descending artery). Infarct size as a proportion of the ischaemic area (IS/AAR) was measured in vivo by myocardial perfusion imaging (MPI) and postmortem by a histochemical procedure (at 150 min of reperfusion). RESULTS: IS/AAR did not differ significantly between control (C), EPO1 and EPO2 groups, neither measured by MPI (mean+/-SD for C: 0.87+/-0.13; EPO1: 0.92+/-0.08; EPO2: 0.87+/-0.11), nor histochemically (mean+/-SD for C: 0.64+/-0.20; EPO1: 0.75+/-0.17; EPO2: 0.80+/-0.07). In the EPO2 group mean arterial pulmonary pressure and dP/dtmax were increased compared with control group. CONCLUSION: Despite promising results from studies in rodents, rhEPO did not reduce infarct size measured after 2.5 h of reperfusion in our porcine model.

Animals↗

PubMed1999

Does beta(3)-adrenoreceptor blockade attenuate acute exercise-induced reductions in leptin mRNA?

We investigated the effect of a single bout of exercise on leptin mRNA levels in rat white adipose tissue. Male Sprague-Dawley rats were randomly assigned to an exercise or control group. Acute exercise was performed on a rodent treadmill and was carried out to exhaustion, lasting an average of 85.5 +/- 1.5 min. At the end of exercise, soleus muscle and liver glycogen were reduced by 88% (P < 0.001). Acutely exercised animals had lower (P < 0.05) leptin mRNA levels in retroperitoneal but not epididymal fat, and this was independent of fat pad weight. To test the hypothesis that beta(3)-adrenergic-receptor stimulation was involved in the downregulation of leptin mRNA in retroperitoneal fat, a second experiment was performed in which rats were randomized into one of four groups: control, control + beta(3)-antagonist, exercise, and exercise + beta(3)-antagonist. A highly selective beta(3)-antagonist (SR-59230A) or vehicle was given by gavage 30 min before exercise or control experiment. Exercise consisted of 55 min of treadmill running, sufficient to reduce liver and muscle glycogen by 70 and 80%, respectively (both P < 0.0001). Again, acute exercise reduced leptin mRNA in retroperitoneal fat (exercise vs. control; P < 0.05), but beta(3)-antagonism blocked this effect (exercise + beta(3)-antagonist vs. control + beta(3)-antagonist; P = 0.42). Unexpectedly, exercise increased serum leptin. This would be consistent with the idea that there are releasable, preformed pools of leptin within adipocytes. We conclude that beta(3)-receptor stimulation is a mechanism by which acute exercise downregulates retroperitoneal adipose tissue leptin mRNA in vivo.

Adipose Tissue↗

PubMed2002

Gap junctions in CO(2)-chemoreception and respiratory control.

Recent evidence indicates that gap junctions play a more prominent role in normal functioning of the mammalian central nervous system (CNS) than was once believed. Accumulating evidence from both neonatal and adult rodents indicates that gap junctions participate in multiple aspects of respiratory control, including central CO(2) chemoreception, respiratory rhythmogenesis, and respiratory motoneuron output. This review provides an overview of gap junction neurobiology in the mammalian CNS and presents the anatomical and electrophysiological evidence for gap junctions in CO(2) chemoreception and respiratory control.

Animals↗

PubMed1994

Multiple loci on human chromosome 11 control tumorigenicity of BK virus transformed cells.

BK virus (BKV) is a human papovavirus that readily transforms rodent cells, but not human cells, to a neoplastic phenotype, suggesting that tumor-suppressor functions expressed in human cells control BKV oncogenicity. Transfer of a normal human chromosome 11 to BKV-transformed mouse cells suppresses the malignant phenotype. In this report we map the regions of chromosome 11 involved in tumor suppression. Transfer of chromosome 11 to the BKV-transformed hamster cell line HKBK produces monochromosomic hybrids retaining only portions of the transferred human chromosome. We have compared the tumorigenicity of the hybrids with the molecular mapping of chromosome 11 retained regions. This analysis indicated that 3 regions of human chromosome 11, 11p15.5, 11p13 and 11q13, cooperate in tumor suppression. However, 11q13 seems the most important, since all the HKBK/H11-induced tumors analysed had lost this region, whereas 11p15.5 and 11p13 were sometimes retained. The chromosomal regions identified in this study are deleted in several types of human tumors, suggesting that the BKV transformation system specifically detects tumor-suppressor genes on chromosome 11 that are involved in human oncogenesis. This model may be of use in isolating and cloning such genes. The results of this report raise the possibility that BKV may have a synergistic tumorigenic effect in human cells where tumor-suppressor genes controlling its oncogenic potential are inactivated.

Animals↗

PubMed2004

Reproduction of the tundra vole (Microtus oeconomus) with dietary phytosterol supplement.

Phytosterols (PS) are plant-derived compounds with estrogenic activity in vitro and beneficial effects on the serum lipid profile in vivo. In nature, PS exposure can derive from pulp mill effluents. The effects of a pulp-mill derived PS mixture on the reproduction, endocrine variables and enzyme activities of the tundra vole (Microtus oeconomus) were investigated in a two-generation study. The cumulative food intake of PS-treated females was higher than in the control group supporting previous results on the effects of PS on food consumption in rodents. 85% of the PS treated pairs reproduced, but the figure was only 60% for the control pairs. The plasma and testicular testosterone concentrations were lower in the adult PS males, but the PS-treated male offspring had higher testicular testosterone concentrations than their controls. In the female offspring, the liver lipase activity was higher in the PS-treated group, which could be a result of decreased cholesterol absorption in the gut. Chronic PS treatment increased the reproduction probability of the species and had a potential effect on the sex steroid hormones of maturing offspring, which could have applications in environmental monitoring.

Administration, Oral↗

PubMed2006

Novel immunoblotting monoclonal antibodies against human and rat CD36/fat used to identify an isoform of CD36 in rat muscle.

CD36, a surface membrane glycoprotein, functions as a class B scavenger receptor that binds to several distinct ligands. Included among these is oxidized low-density lipoprotein (Ox-LDL), a major trigger of atherosclerotic lesions, and the levels of CD36 activity and Ox-LDL uptake may have an impact on coronary artery disease. In addition, recent studies in rodents have shown that CD36, also known as FAT, controls the levels of free fatty acids and triglycerides in plasma, and is an important regulator of the metabolic pathways involved in insulin resistance. Despite the importance of measuring CD36 expression in different tissues there is a paucity of good immunoblotting antibodies, particularly for rodent tissue. Here, using GST-fusion proteins incorporating the cysteine cluster encoded by exons VIII, IX, and X of the CD36 gene as immunogen, we have generated a panel of monoclonal antibodies that are excellent blotting reagents for human and rat CD36. With these reagents we were able to visualize an additional, faster migrating CD36 band in rat muscle, likely representing a minor splice variant of CD36 (CD36var.1) hitherto seen only in the human HEL cell line.

Amino Acid Sequence↗

PubMed1998

A new highly specific method for predicting the carcinogenic potential of pharmaceuticals in rodents using enhanced MCASE QSAR-ES software.

This report describes in detail a new quantitative structure-activity relational expert system (QSAR-ES) method for predicting the carcinogenic potential of pharmaceuticals and other organic chemicals in rodents, and a beta-test evaluation of its performance. The method employs an optimized, computer-automated structure evaluation (MCASE) software program and new database modules which were developed under a Cooperative Research and Development Agreement (CRADA) between FDA and Multicase, Inc. The beta-test utilized 126 compounds with carcinogenicity studies not included in control database modules and three sets of modules, including: A07-9 (Multicase, Inc.), AF1-4 (FDA-OTR/Multicase, Inc.), and AF5-8 (FDA-OTR/proprietary). The investigation demonstrated that the standard MCASE(A07-9) system which had a small data-set (n = 319), detected few structure alerts (SA) for carcinogenicity (n = 17), and had poor coverage for beta-test compounds (51%). Conversely, the new, optimized FDA-OTR/MCASE(AF5-8) system had a large data-set (n = 934), detected many SA (n = 58) and had good coverage (94%). In addition, the study showed the standard MCASE(A07-9) software had poor predictive value for carcinogens and specificity for noncarcinogens (50 and 42%), detected many false positives (58%), and exhibited poor concordance (46%). Conversely, the new, FDA-OTR/MCASE(AF5-8) system demonstrated excellent predictive value for carcinogens and specificity for non-carcinogens (97%, 98%), detected only one false positive (2%), and exhibited good concordance (75%). The dramatic improvements in the performance of the MCASE were due to numerous modifications, including: (a) enhancement of the size of the control database modules, (b) optimization of MCASE SAR assay evaluation criteria, (c) incorporation of a carcinogenic potency scale for control compound activity and MCASE biophores, (d) construction of individual rodent gender- and species-specific modules, and (e) defining assay acceptance criteria for query and control database compounds.

Animals↗

PubMed1984

Genetic and environmental influences on developing autonomic control of heart rate.

Individual differences in cardiovascular regulation result from a dynamic interaction between genetically programmed developmental processes and extrinsic (environmental) conditions. The alterations in autonomic functioning previously identified among pups of the spontaneously hypertensive rat (SHR) strain suggest a genetic influence on autonomic development. In the present studies, an early stimulation procedure previously shown to reduce the behavioral and endocrine responsiveness of rodents in adulthood was demonstrated to alter both neural control of heart rate and regional brain catecholamine levels during the preweaning period. Pups from litters of SHR and Wistar-Kyoto (WKY) rats were handled daily during the first postnatal week. Selective pharmacological blockade with atenolol and atropine methylnitrate was used to identify autonomic controls of heart rate at 16 and 28 days of age. Combined blockade was used to estimate intrinsic heart rate. In both SHR and WKY, early handling was associated with elevated basal heart rate, elevated intrinsic heart rate, and decreased sympathetic tone. Parasympathetic influence on heart rate was elevated by early handling in WKY and decreased by handling in SHR. In addition, an increase in dorsal cortical norepinephrine concentration was produced by early handling in both strains. These data suggest that early environmental conditions can interact with the genetic predisposition for elevated blood pressure and may play a potentially important role in organizing the neural controls of cardiovascular regulation.

Adrenergic beta-Antagonists↗

PubMed2006

Survey of lymphocytic choriomeningitis virus diagnosis and testing--Connecticut, 2005.

Lymphocytic choriomeningitis virus (LCMV) is a rodent borne virus that can be transmitted to humans through exposure to rodent urine, feces, saliva, or blood. LCMV infection is often asymptomatic or mild but can cause aseptic meningitis, encephalitis, life-threatening infections in immunosuppressed persons, and severe congenital defects . In May 2005, LCMV was implicated in the deaths of three organ transplant recipients who had received organs from a common donor who had likely been infected from a pet rodent. In August 2005, the Connecticut Department of Public Health conducted surveys of hospital laboratories and infectious disease (ID) physicians in Connecticut to determine recent incidence of confirmed LCMV infection, the level of awareness of LCMV, and the frequency of LCMV testing. This report summarizes the results of those surveys, which indicate that awareness of LCMV is high among ID physicians; however, testing for LCMV is infrequent, and ID physicians might not be aware of the need to consider LCMV among the most susceptible populations even when a history of rodent contact is not initially evident. In part because of these findings, LCMV infection is now a physician- and laboratory-reportable disease in Connecticut. More systematic efforts are needed to determine the frequency of LCMV infection and to monitor for pet rodent infection.

Clinical Laboratory Techniques↗

PubMed1994

Bolivian hemorrhagic fever--El Beni Department, Bolivia, 1994.

In July 1994, an outbreak of Bolivian hemorrhagic fever (BHF), which is caused by Machupo virus, began in northeastern Bolivia. This report describes the investigation and features of this outbreak, the search for additional cases of BHF in El Beni, Bolivia, and results of rodent investigations.

Adolescent↗

PubMedDate not supplied

Reversible hippocampal lesions disrupt water maze performance during both recent and remote memory tests.

Conventional lesion methods have shown that damage to the rodent hippocampus can impair previously acquired spatial memory in tasks such as the water maze. In contrast, work with reversible lesion methods using a different spatial task has found remote memory to be spared. To determine whether the finding of spared remote spatial memory depends on the lesion method, we reversibly inactivated the hippocampus with lidocaine either immediately (0-DAY) or 1 mo (30-DAY) after training in a water maze. For both the 0-DAY and 30-DAY retention tests, rats that received lidocaine infusions exhibited impaired performance. In addition, when the 0-DAY group was retested 2 d later, (when the drug was no longer active), the effect was reversed. That is, rats that had previously received lidocaine performed as well as control rats did. These findings indicate that the rodent hippocampus is important for both recent and remote spatial memory, as assessed in the water maze. What determines whether remote spatial memory is preserved or impaired following disruption of hippocampal function appears to be the type of task used to assess spatial memory, not the method used to disrupt the hippocampus.

Anesthetics, Local↗

PubMed1989

Impaired control of respiration in iron-deficient muscle mitochondria.

Dietary iron deficiency (ID) decreases iron-containing proteins and hence respiratory capacity of skeletal muscle mitochondria (SMM), but noniron components are much less affected. Using a hexokinase plus glucose ATP-utilizing system, we studied control of respiration in isolated SMM from rats of variable iron status: ID, ID 3 days after intraperitoneal treatment with iron dextran, and control. We found that sensitivity of respiratory control (e.g., ATP/ADP at a given oxygen consumption) was positively related to state 3 respiratory capacity. Titration studies with carboxyatractyloside, a noncompetitive inhibitor of adenine nucleotide translocase (AdNT), revealed that AdNT concentration was unaffected by iron status. However, the turnover number of AdNT was markedly reduced by ID and improved with iron treatment. We conclude that in ID SMM, decreased maximal respiratory capacity is paralleled by impaired sensitivity to putative controllers of oxidative phosphorylation at any respiratory rate, despite normal levels of AdNT. A second study was designed to determine possible consequences of impaired sensitivity of respiratory control on motor unit recruitment during exercise. ID and normal rats were subjected to a program of walking treadmill exercise. Although exercise failed to induce any changes in oxidative enzyme levels in control rat, ID animals and exhibited substantial mitochondrial enzyme adaptation in hindlimb skeletal muscle. Furthermore, the most consistent enzymatic changes were observed to occur in fast glycolytic muscle fibers. These results suggest marked alterations in the pattern of muscle fiber recruitment during mild exercise in ID rodents and support the hypothesis that sensitivity of respiratory control in SMM is an important determinant of motor unit recruitment during aerobic exercise.

Adenosine Diphosphate↗

PubMed1997

An alternative approach for investigating the carcinogenicity of indoor air pollution: pets as sentinels of environmental cancer risk.

Traditionally, the cancer risks associated with radon,environmental tobacco smoke (ETS), and similar indoor residential exposures have been evaluated through either laboratory experiments in rodents or epidemiology studies in people. Laboratory studies have the advantage of being controlled experiments, but their utility as estimators of human risk is limited by the uncertainties of extrapolating from rodents to people and from high doses to those typically experienced in the home. These experiments also subject animals to noxious exposures, causing suffering that may be considered cruel. Traditional epidemiology studies evaluate human risk directly, at the exposure levels present in residences; however, these studies are limited by their potential for misclassification, biased recall, and uncontrolled confounding. The long time intervals involved between exposure and disease (often 30 years or more) make accurate recall particularly problematic. In this paper we discuss the limitations of these traditional approaches, especially as they relate to residential studies of radon and ETS. The problems associated with the maximum tolerated dose in rodent bioassays and exposure misclassification in traditional epidemiology are particularly examined. A third approach that supplements the traditional approaches and overcomes some of their limitations is suggested. This approach, dubbed pet epidemiology, estimates residential cancer risk by examining the exposure experience of pet dogs with naturally occurring cancers. The history of pet epidemiology is reviewed and its strengths and limitations are examined.

Air Pollution, Indoor↗

PubMed2006

The hypothalamic H1 receptor: a novel therapeutic target for disrupting diurnal feeding rhythm and obesity.

Histamine-containing neurons and histamine H1 receptors are distributed within the brain and peripheral tissues. The results of physiological and pharmacological studies have revealed that brain histamine and H1 receptors are involved in the regulation of feeding and obesity in rodents. The adipocytokine leptin regulates feeding and obesity, partially through brain histamine. Furthermore, recent studies have provided evidence that regulation of the diurnal rhythm of feeding through H1 receptors is a crucial factor in the development of obesity. Thus, the regulation of H1 receptors is important for the control of energy metabolism, feeding rhythms and obesity in rodents.

Animals↗

PubMed2002

Brain evolution and lifespan regulation: conservation of signal transduction pathways that regulate energy metabolism.

Mechanisms for sensing, acquiring, storing and using energy are fundamental to the survival of organisms at all levels of the phylogenetic scale. Single-cell organisms evolved surface receptors that sense an energy source and, via signal transduction pathways that couple the receptors to the cell cytoskeleton move towards the energy source. Mutlicellular organisms evolved under conditions that favored species that developed complex mechanisms for obtaining food, with nervous systems being critical mediators of energy acquisition and regulators of energy metabolism. A conserved signaling system involved in regulating cellular and organismal energy metabolism, and in sensing and responding to energy/food-related environmental signals, involves receptors coupled to the phosphatidylinositol-3-kinase-Akt signaling pathway. Prominent activators of this pathway are insulin, insulin-like growth factors and brain-derived neurotrophic factor (BDNF). Recent studies in diverse organisms including nematodes, flies and rodents have provided evidence that insulin-like signaling in the nervous system can control lifespan, perhaps by modulating stress responses and energy metabolism. Interestingly, the lifespan-extending effect of dietary restriction in rodents is associated with increased BDNF signaling in the brain, and a related increase of peripheral insulin sensitivity, suggesting a mechanism whereby the brain can control lifespan. Thus a prominent evolutionarily conserved function of the nervous system is to regulate food acquisition and energy metabolism, thereby controlling lifespan.

Animals↗

PubMed1984

Somatic cell genetic analysis of human cell surface antigens: chromosomal assignments and regulation of expression in rodent-human hybrid cells.

The expression of 13 newly defined human cell surface antigens identified by monoclonal antibodies was studied in a panel of reduced rodent-human somatic cell hybrid clones. For each antigenic system the segregation of antibody reactivity was concordant with the segregation of a specific human chromosome, permitting the chromosomal assignment of 13 gene loci determining antigen expression. The antigens can be placed in four groups on the basis of their patterns of control in the hybrid cells. (i) Presence of a single human chromosome is necessary and sufficient for antigen expression; L230 (assigned to chromosome 2), AJ425, K15 (chromosome 3), SR84 (chromosome 5), JF23, Q14 (chromosome 11), SV13 (chromosome 15), and F10 (chromosome 19). (ii) AJ2 (chromosome 10) and J143 (chromosome 17); two antigens coded for by separate human chromosomes but associated as a molecular complex on the surface of AJ2+/J143+ human cells. (iii) F8 (chromosome 19); antigen expression dependent on the growth characteristics of hybrid cells: substrate-adherent cells are F8+, whereas cells growing in suspension are F8-. (iv) AO122 and F23 (chromosome 15); antigen expression controlled by the permissive/inducing vs. nonpermissive/noninducing nature of the rodent fusion partner. Hybrids derived from both antigen-positive and antigen-negative human cells can express AO122 and F23 but only when specific rodent cell types are used for hybridization: N4TG-1 neuroblastoma and L cells, but not RAG renal carcinoma cells, permit AO122 expression, whereas RAG and L cells, but not N4TG-1 cells, permit F23 expression. The rapidly expanding list of monoclonal antibodies defining human cell surface molecules provides a range of markers to probe the genetic regulation of antigen diversity in somatic cells.

Animals↗

PubMed1993

Development and longevity of Nosopsyllus laeviceps kuzenkovi (Siphonaptera) from Inner Mongolia under laboratory conditions.

The development and longevity of Nosopsyllus laeviceps kuzenkovi (Yagubyants), a major plague vector among sylvan and campestral rodents in Inner Mongolia, China, was studied under controlled laboratory conditions of 11, 14, 17, 20, 23, 26, 29, and 35 C at 76% relative humidity (R.H.), and 32, 53, 76, 87, and 100% at 23 C. Development from egg to adult was shortest (21-23 days) under favorable conditions of 26 C at 76% R.H., but maximum survival to adulthood (84%) occurred at 23 C. Average longevity was 13.25 days (13.70 in females and 12.80 in males) at 17 C and 76% R.H.; it was longer at cooler and shorter at warmer temperatures. Findings provided experimental data that helped clarify seasonal fluctuations, summer mortality, generation cycles, and survival of compared flea species from Russia, Azerbaidzhan, and China.

Animals↗