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PubMedDate not supplied

Sex differences in naloxone- and Tyr-MIF-1-induced hypoalgesia.

Reproductive adult male and female deer mice that received daily (7 days) injections of either the prototypic exogenous opiate antagonist, naloxone (1.0 mg/kg), or the endogenous putative antiopioid tetrapeptide, Tyr-MIF-1 (Tyr-Pro-Leu-Gly amide; 1.0 and 10 mg/kg), followed by determinations of thermal nociceptive sensitivity (hot-plate response) developed hypoalgesia. There were significant sex differences in this opioid blockade-induced or associated analgesia, with male mice displaying significantly greater hypoalgesia than females. Mice that received daily injections of either naloxone or Tyr-MIF-1 for 7 days without any accompanying determinations of nociceptive sensitivity (days 2-6 of treatment) failed to show any hypoalgesia on day 7 when they received the antagonist followed by a measurement of nociception. These results indicate that there are sex differences in both naloxone- and Tyr-MIF-1-induced hypoalgesia, and suggest that this pattern may be associated with sexually dimorphic opioid modulation of aversive conditioning.

Animals↗
PubMed1984

Shrew metabolic rates and thyroxine utilization.

Elevated basal metabolic rates (BMR) in shrews have been observed for over 40 years, yet no one has investigated the physiological basis for this phenomenon. This paper reports on investigations of thyroid function in a shrew (Sorex vagrans), and in three rodent species for comparison. The utilization rate of thyroxine in shrews is found to be much higher than for any of the rodents, and is correlated with BMR expressed as a percentage of the predicted BMR. It is concluded that the unusually high thyroxine utilization rates of Sorex are an important, if not the sole, determinant of their elevated metabolic rates.

Animals↗
PubMed1986

Photoperiodic adjustment of thermal conductance in deer mice.

Seasonal changes in metabolic rate can be induced in mice held in thermal neutral (26-29 degrees C) ambient temperatures. The metabolic effect of winter photoperiod is a lower metabolic rate without compromise to metabolic reserve. Manipulations of photoperiod or melatonin backgrounds adjust the thermoregulatory setting for core temperature level and affect thermal conductance.

Acclimatization↗
PubMed1988

Pineal melatonin content in photoperiodically responsive and non-responsive phenotypes of deer mice.

1. The pineal melatonin content of photoperiod responsive and photoperiod non-responsive male deer mice was assessed. 2. Pineal melatonin content did not differ between short-day mice with regressed testes or those that maintained their reproductive systems. 3. These data suggest that differential phasing of melatonin release or post-pineal mechanisms are responsible for the differential responsiveness to day length among deer mice.

Animals↗
PubMed1995

Distribution of fasciolosis in Kansas, with results of experimental snail susceptibility studies.

A total of 278 veterinarians throughout Kansas were sent mail-in survey forms asking specific questions relating to their experience with fasciolosis in their practice area. Replies were received from 178 (64%) veterinarians representing six practice types; one-third reported having seen cases of fasciolosis in their practice. The results of our survey indicate that the majority of the cattle diagnosed with liver fluke disease in Kansas are imported from other areas of the USA. However, in both central and southeastern regions of Kansas, some cattle that had never been out of the state were infected with Fasciola hepatica. Thus, these areas of Kansas should be considered endemic for liver fluke disease. Methods of diagnosis, types of operations, and improvements seen after treatment were also discussed. In order to ascertain the existence of one or more possible snail intermediate hosts within Kansas, five species of lymnaeid snails were collected from central and southeastern parts of the state and tested for their susceptibility to infection by Fasciola hepatica. The snails collected included Pseudosuccinea columella, Fossaria obrussa, Fossaria bulimoides, Fossaria parva and Fossaria dalli. Of these, Pseudosuccinea columella and Fossaria bulimoides proved susceptible to experimental infection by Fasciola hepatica. Metacercariae obtained from experimentally infected snails were used to infect both a weanling calf thereby completing the life cycle of the parasite. This report is the first to identify the existence of suitable snail intermediate hosts for Fasciola hepatica in Kansas.

Animals↗
PubMed1982

Comparative study of monoamine levels in discrete brain areas of five rodent species.

1. Dopamine, norepinephrine, serotonin and 5-hydroxyindol-acetic acid levels were studied in discrete brain areas of four wild rodent species and compared with those of laboratory mouse. 2. Monoamine levels showed significant differences in all the species studied. 3. Although it is not possible to exclude the changes induced by the captivity's stress, the results suggest that the natural hypoxic environment (high altitude) and/or the natural diet play an important role on the activity of the monoaminergic neurons. 4. Species which showed a better behavioral pattern of adaptation also showed significant differences in brain monoamine levels.

Animals↗
PubMed1992

Induction of peroxisomes by treatment with perfluorooctanoate does not increase rates of H2O2 production in intact liver.

Increases in acyl coenzyme A (CoA) oxidase activity due to peroxisome proliferation are postulated to cause oxidative stress via elevated production of H2O2, leading to DNA damage. These changes are suspected to be responsible for tumor formation caused by non-genotoxic carcinogens which do not bind to DNA but cause proliferation of peroxisomes. However, the activity of the peroxisomal enzyme acyl CoA oxidase assayed in vitro in the presence of excess fatty acyl CoA substrate may not reflect rates of H2O2 generation in intact liver where fatty acid supply is carefully controlled in part by delivery of substrate. The purpose of this work was to determine if rates of hepatic H2O2 generation were altered in perfused liver and in vivo following induction of H2O2-generating acyl CoA oxidase activity. Injection of the potent peroxisome proliferating agent perfluorooctanoate into rats 5 days prior to sacrifice caused an expected 4-fold increase of H2O2-generating acyl CoA oxidase activity measured in hepatic homogenates. In contrast, rates of H2O2 generation in perfused liver measured spectrophotometrically (660-640 nm) through a lobe of the liver were not altered by perfluorooctanoate treatment (7.3 +/- 1.5 vs. 7.8 +/- 0.5 mumol/g/h in livers from untreated control rats). Similar treatment with perfluorooctanoate also increased in vitro acyl CoA oxidase activity 9-fold in livers from deermice; however, rates of elimination of methanol, a selective substrate for catalase in rodents whose oxidation is limited by the supply of H2O2, were not altered significantly in vivo (control, 110 +/- 11 mumol/g/h vs. perfluorooctanoate, 112 +/- 32 mumol/g/h). Taken together, these data demonstrate that elevation of H2O2 formation by acyl CoA oxidase activity measured in vitro is not necessarily associated with increases in rates of H2O2 generation in intact perfused liver or in vivo, most likely due to rate-limitation in intact cells by fatty acid supply. These data do not support the hypothesis that the induction of peroxisomes leads to excessive H2O2 production and oxidative stress. It follows that alternative hypotheses to explain carcinogenesis caused by peroxisome-proliferating agents need to be considered.

Animals↗
PubMedDate not supplied

In vivo roles of alcohol dehydrogenase (ADH), catalase and the microsomal ethanol oxidizing system (MEOS) in deermice.

The relative importance of ADH and MEOS for ethanol oxidation in the liver has yet to be elucidated. The discovery of a strain of deermice genetically lacking ADH (ADH-) which can consume ethanol at greater than 50% of the rates seen in deermice having ADH (ADH+) suggested a significant role for non-ADH pathways in vivo. To quantitate contributions of the various pathways, we examined first the ethanol oxidation rates with or without 4-methylpyrazole in isolated deermice hepatocytes. 4-Methylpyrazole significantly reduced the ethanol oxidation in both ADH+ and ADH- hepatocytes. The reduction seen in ADH- cells can be applied to correct for the effect of 4-methylpyrazole on non-ADH pathways of ADH+ deermouse hepatocytes. After correction, non-ADH pathways were found to contribute 28% of ethanol metabolism at 10 mM and 52% at 50 mM. When using a different approach namely measurement of the isotope effect, MEOS was calculated to account for 35% at low and about 70% at high blood ethanol concentrations. Thus, we found that two different complementary approaches yielded similar results, namely that non-ADH pathways play a significant role in ethanol oxidation even in the presence of ADH.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Effects of acute ethanol administration and chronic ethanol feeding on mixed function oxidation in deermice lacking ADH.

Hepatic microsomes catalyze the oxidation of ethanol and other drugs. The mechanisms through which ethanol alters mixed function oxidation are still debated. There is evidence that ethanol and drugs interact at a microsomal level, but there are also claims that ethanol may interfere with drug metabolism indirectly by affecting the supply of NADPH through NADH production in the ADH pathway. To investigate the role of chronic ethanol consumption, deermice with normal liver ADH (ADH+) or genetically lacking ADH (ADH-) were pair-fed liquid diets containing ethanol or isocaloric carbohydrate for 23 days. The acute effects of ethanol were studied in deermice fed standard laboratory chow and tap water ad lib. In vivo and in vitro, the effects of an acute dose of ethanol and chronic ethanol feeding on mixed function oxidation as measured by the demethylation of aminopyrine were similar in both animal strains. Statistical analysis showed no significant differences between ADH+ and ADH- animals under all experimental conditions studied. We conclude that induction and inhibition of mixed function oxidation by ethanol may be related to the interaction of ethanol with hepatic microsomes rather than to redox changes produced by ADH mediated ethanol metabolism.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate concentrations in blood and tissues of mice fed ethanol-containing liquid diets.

The effects of chronic ethanol administration on vitamin B-6 metabolism were studied in female Long-Sleep (LS) and Short-Sleep (SS) mice. Animals were fed an ethanol containing liquid diet (AIN-76) for four weeks. Concentration of ethanol in the diet increased from 10 to 25% ethanol-derived calories (EDC) during weeks 1-3 and was maintained at 30% EDC for 1 additional week. We measured concentrations of pyridoxal 5'-phosphate (PLP) in plasma, erythrocytes and whole blood, and liver and brain PLP and pyridoxamine 5'-phosphate (PMP) in ethanol-fed and pair-fed control mice. Chronic ethanol administration significantly increased PMP and total (PLP + PMP) levels in the liver of SS mice. In LS mice ethanol feeding significantly decreased PMP and total (PLP + PMP) levels in the brain, but these values were still within normal limits. These results suggest that both control and ethanol-containing liquid diets are nutritionally adequate with respect to vitamin B-6, and that chronic ethanol administration does not adversely affect vitamin B-6 metabolism in adult mice.

Animals↗
PubMed1986

Central metabolism of beta-endorphin in different species of temperature acclimated rodents.

The purpose of this study was to characterize the central metabolism/processing of beta-endorphin in wild, desert rodents and to study the effect of heat and cold acclimation on central metabolism/processing and beta-endorphin half-life. This report suggests that a shift occurs in the processing of beta-endorphin in desert rodents acclimated to heat and cold leading to an accumulation of gamma-type endorphins. The data support a significant difference in beta-endorphin half-life between the rodents and the laboratory white rat.

Acclimatization↗
PubMed1988

Differential effects of adrenergic blockade on seasonal changes in core temperatures and thermal conductances of deer mice maintained in thermal neutral environments.

1. Resting, daytime, thermal conductances and metabolic rates of mice conditioned to winter (10:14LD) and summer (14:10LD) photoperiods were reduced by social huddling; huddling resulted in group size related elevations in core temperature during summer, but not with winter light-dark cycle exposures. 2. Core temperatures of resting, solitary winter animals were lower than those of summer; both summer and winter animals' core temperatures were further reduced by increased thermal conductance resulting from (phentolamine) alpha receptor blockade. 3. Social huddling reduction of the heat loss from phentolamine treatment was more effective for winter (10:14LD) animals. 4. While phentolamine treatment resulted in increased thermal conductance and lower core temperatures of the mice, propranalol treatment resulted in lower core temperatures and resting metabolic rates, with a resulting decrease in thermal conductance. 5. Since adrenergic blockade was less dose-effective on winter animals, we reasoned that winter animals display higher levels of endogenous adrenergic capacity than summer animals and that lower winter thermoregulatory set points provide for energy conservation with enhanced capacity for meeting cold challenge.

Animals↗
PubMed2006

Metabolic basis of ethanol-induced hepatic and pancreatic injury in hepatic alcohol dehydrogenase deficient deer mice.

Alcoholic liver disease (ALD) and alcoholic pancreatitis (AP) are major diseases causing high mortality and morbidity among chronic alcohol abusers. Neutral lipid accumulation (steatosis) is an early stage of ALD or AP and progresses to inflammation and other advanced stages of diseases in a subset of chronic alcohol abusers. However, the mechanisms of alcoholic steatosis leading to ALD and AP are not well understood. Chronic alcohol abuse impairs hepatic alcohol dehydrogenase (ADH, a major enzyme involved in ethanol oxidative metabolism) and facilitates nonoxidative metabolism of ethanol to fatty acid ethyl esters (FAEEs, nonoxidative metabolites of ethanol). These esters are implicated in the pathogenesis of various alcoholic diseases and shown to cause hepatocellular and pancreatitis-like injury. Ethanol exposure is known to increase synthesis of FAEEs by several-fold in the livers and pancreata of rats pretreated with hepatic ADH inhibitor. Therefore, studies were undertaken to evaluate hepatocellular and pancreatic injury in hepatic ADH-deficient (ADH(-)) deer mice versus ADH-normal (ADH(+)) deer mice fed ethanol (4% wt/vol) via Lieber-DeCarli liquid diet for 60 days. A significant mortality was found in ethanol-fed ADH(-) deer mice (11 out of 18) versus ADH(+) deer mice (1 out of 16); most of the deaths occurred during the first 2 weeks of ethanol exposure. The surviving animals, sacrificed at the end of 60th day, showed distinct changes in hepatic and pancreatic histology and several-fold increases in nonoxidative metabolism of ethanol in ethanol-fed ADH(-) versus ADH(+) deer mice. Extensive vacuolization with displacement or absence of nucleus in some hepatocytes, and significant increase in hepatic neutral lipids were found in ethanol-fed ADH(-) versus ADH(+) deer mice. Ultrastructural changes showed perinuclear space, edema, presence of apoptotic bodies and disintegration, and/or dilatation of endoplasmic reticulum (ER) in the pancreata of ethanol-fed ADH(-) deer mice. FAEE levels were significantly higher in ADH(-) versus ADH(+) deer mice, approximately four-fold increases in the livers and seven-fold increases in the pancreata. Ethyl esters of oleic, linoleic, and arachidonic acids were the major FAEEs detected in ethanol-fed groups. The role of FAEEs in pancreatic lysosomal fragility is reflected by higher activity of cathepsin B (five-fold) in ethanol-fed ADH(-) versus ADH(+) deer mice. Although the present studies clearly indicate a metabolic basis of ethanol-induced hepatic and pancreatic injury, detailed dose- and time-dependent toxicity studies in this ADH(-) deer mouse model could reveal further a better understanding of mechanism(s) of ethanol-induced hepatic and pancreatic injuries.

Alcohol Dehydrogenase↗
PubMed2005

Striatal opioid peptide content in an animal model of spontaneous stereotypic behavior.

Stereotypic behaviors are associated with a broad spectrum of developmental, psychiatric, and genetic disorders. Several lines of evidence indicate that these abnormal repetitive behaviors may be expressed as a consequence of imbalanced activity along the direct and indirect processing pathways of the basal ganglia. Because the activity of these two pathways is modulated, in part, by the neuropeptides dynorphin and enkephalin, we sought to determine whether spontaneous and persistent stereotypy is associated with alterations in striatal neuropeptide content. Specifically, the present study employed radioimmunoassay to measure dynorphin-A and leu-enkephalin content in the dorsolateral striatum of deer mice exhibiting different levels of spontaneous stereotypic jumping. The results indicate significantly decreased leu-enkephalin content and significantly increased dynorphin/enkephalin content ratios in high-stereotypy mice relative to low-stereotypy mice. Moreover, analyses revealed a significant negative correlation between striatal enkephalin content and frequency of stereotypy as well as a significant positive correlation between the dynorphin/enkephalin content ratio and frequency of stereotypy in these mice. These data are consistent with the hypothesis that spontaneous stereotypic behavior is expressed as a consequence of relative hyperactivity along cortico-basal ganglia-cortical feedback circuits involving the direct (facilitative) pathway, but suggest that primary perturbations to the indirect (inhibitory) pathway give rise to such imbalanced activity.

Animals↗
PubMed2006

Animal models of restricted repetitive behavior in autism.

Restricted, repetitive behavior, along with deficits in social reciprocity and communication, is diagnostic of autism. Animal models relevant to this domain generally fall into three classes: repetitive behavior associated with targeted insults to the CNS; repetitive behavior induced by pharmacological agents; and repetitive behavior associated with restricted environments and experience. The extant literature provides potential models of the repetitive behavioral phenotype in autism rather than attempts to model the etiology or pathophysiology of restricted, repetitive behavior, as these are poorly understood. This review focuses on our work with deer mice which exhibit repetitive behaviors associated with environmental restriction. Repetitive behaviors are the most common category of abnormal behavior observed in confined animals and larger, more complex environments substantially reduce the development and expression of such behavior. Studies with this model, including environmental enrichment effects, suggest alterations in cortical-basal ganglia circuitry in the development and expression of repetitive behavior. Considerably more work needs to be done in this area, particularly in modeling the development of aberrant repetitive behavior. As mutant mouse models continue to proliferate, there should be a number of promising genetic models to pursue.

Animals↗
PubMed2004

Perchlorate in water, soil, vegetation, and rodents collected from the Las Vegas Wash, Nevada, USA.

Water, soil, vegetation, and rodents were collected from three areas along the Las Vegas Wash, a watershed heavily contaminated with perchlorate. Perchlorate was detected at elevated concentrations in water, soil, and vegetation, but was not frequently detected in rodent liver or kidney tissues. Broadleaf weeds contained the highest concentrations of perchlorate among all plant types examined. Perchlorate in rodent tissues and vegetation was correlated with perchlorate concentrations in soil as expected, however rodent residues were not highly correlated with plant perchlorate concentrations. This indicates that soil may be a greater source, or a more constant source of perchlorate exposure in rodents than vegetation.

Animals↗