Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune reactivity of primiparous pregnant C57Bl/6J mice was investigated using in vitro assays of mitogen reactivity. The response to the T cell mitogens phytohemagglutinin (PHA) and concanavalin A of cells from the paraaortic (PA) lymph nodes, which drain the uterus, was decreased in pregnant animals. Reactivity to lipopolysaccharide, a B cell mitogen, was normal. The decreased PHA response was seen with PA cells from mice bearing syngeneic or allogeneic (to DBA/2J) fetuses. It was not due to a change in sensitivity to PHA dose or to active suppression (as demonstrated by mixing experiments). Phytohemagglutinin reactivity of cells from inguinal nodes of pregnant mice showed a more variable depression of response in comparison to that seen with cells from the draining PA nodes. The response of axillary and brachial node cells was similar to virgin values. Statistical analysis revealed no differences in the average number of PA lymphocytes or fetuses per mouse between mice bearing syngeneic or allogeneic fetuses. This parallels the similarities found between syngeneic and allogeneic matings in in vitro functional assays. This study demonstrates that pregnant mice (syngeneic or allogeneic) show only a decrease in T proliferative capacity localized to the area of the uterus, while such responses in the rest of the body are left essentially intact.
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PMID:Cellular immunity during pregnancy. II. Response to T and B cell mitogens. 697 82

DBA/2 mice, 12 days after infection with the polycythemia-inducing Friend virus (F-MulV-P), were treated with a single dose of BCNU. The effect of 35 mg/kg and lower doses on the different stem cell pools (CFUS, CFUC, CFUE) and the F-MulV-P specific ICPC (infectious centers producing cells) and Ep-independent CFUE was studied in detail. The depression of CFUS and CFUC was comparable in normal and F-MuLV-P infected mice. The CFUE population of virus infected mice, which had been completely Ep independent before treatment, showed only some normal Ep dependent colony growth thereafter. This finding was in contrast to the effect of multiple doses of Hydroxyurea, studied previously, which had given the same quantitative depression of CFUS and CFUC. Possible reasons for this failure are discussed; they may be the more proliferation independent mode of action of BCNU and the delayed hemopoietic regeneration.
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PMID:Hematopoietic stem cells in Friend murine leukemia virus infected mice undergoing chemotherapy: failure to eradicate Ep-independent erythropoiesis by BCNU. 706 Jun 65

A single injection of pristane was given i.p. to plasmacytoma-susceptible BALB/cAn mice. At intervals up to 6 mo thereafter, immunofluorescence labeling of intranuclear terminal deoxynucleotidyl transferase (TdT), cell surface B220 glycoprotein, cytoplasmic mu-chains of IgM (c mu), and surface mu-chains (s mu), together with mitotic arrest techniques, were used to quantitate the in vivo population dynamics of precursor B cells in the bone marrow. TdT-expressing pro-B cells (TdT+B220-, TdT+B220+), before the expression of mu-chains, showed sustained increases in both population size and the number of cells flowing through mitosis per unit time. In contrast, populations of pre-B cells (c mu + s mu -) and B cells (s mu +) were consistently depressed for long periods of time, including the phase of plasmacytoma formation. Precursor B cells in DBA/2 mice, a plasmacytoma-resistant strain, showed similar responses to pristane treatment. The results demonstrate that a single injection of pristane, which greatly increases the demand for macrophage activity in the peritoneal space, causes sustained distant alterations in B cell lymphopoiesis in the bone marrow; specifically, a prolonged increased proliferation of pro-B cells coupled with a depression and a exaggerated loss of pre-B cells and B cells. The protracted stress on B cell lymphopoiesis may be a predisposing factor in the subsequent development of c-myc-activating chromosomal rearrangements that play a critical role in plasmacytomagenesis.
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PMID:Perturbation of B cell genesis in the bone marrow of pristane-treated mice. Implications for plasmacytoma induction. 786 85

Bulbectomy has been previously shown to produce the specific antidepressant-sensitive syndrome in C57Bl/6j, but not DBA/2j mice. The present study examined the effect of the depression on voluntary alcohol consumption. Alcohol consumption and alcohol preference (% of alcohol solution in total liquid) in a free-choice, two-bottle situation was measured in C57BL/6j and DBA/2j mice after sham-operation, anosmia with 10% ZnSO4, or bulbectomy. Both anosmic and bulbectomized mice of both strains consumed more alcohol and showed stronger preference for alcohol than sham-operated mice. In DBA/2j mice both operations altered alcohol consumption of the whole population, and the effect of bulbectomy was stronger. In C57Bl/6j mice bulbectomy and, to a less degree, anosmia seemed to affect predominantly the low-drinking animals. Chronic treatment with antidepressants amitriptyline (20 mg/kg), trazodone (20 mg/kg), and imipramine (10 mg/kg), did not change alcohol consumption in sham-operated C57Bl/6j mice. In anosmic mice antidepressants decreased alcohol preference, but only amitryptyline also decreased alcohol consumption. All antidepressants decreased both alcohol consumption and preference in bulbectomized C57Bl/6j mice. In DBA/2j mice antidepressant treatment either increased, or did not alter alcohol consumption and preference in all groups, though the effects varied among individual antidepressants. The possible connection between the bulbectomy-induced behavioral syndrome and elevated ethanol consumption in C57Bl/6j mice is discussed.
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PMID:Antidepressants suppress bulbectomy-induced augmentation of voluntary alcohol consumption in C57B1/6j but not in DBA/2j mice. 797

A water extract of the West African black pepper Piper guineense L. was tested for activity against audiogenic seizures in DBA/2 mice, and against seizures induced in T.O. mice by N-methyl-DL-aspartate (NMDLA), pentylenetetrazole (PTZ) and maximal electroschock. Single intraperitoneal doses of the extract produced significant protection of DBA/2 mice against audiogenic seizures. The highest of three doses tested produced 100% and 58% protection at 6 h and 18 h after treatment, respectively. The extract also protected T.O. mice against convulsions induced by NMDLA and maximal electroshock but it had no significant effect on PTZ-induced convulsions. The doses of the extract tested did not cause significant impairment of performance of T.O. mice on a rotarod test. The results indicate that the extract of P. guineense has prolonged anticonvulsant activity at doses which do not cause significant CNS depression.
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PMID:Anticonvulsant effects of extracts of the west African black pepper, Piper guineense. 841 44

In susceptible DBA/2 mice coxsackievirus B 3-induced myocarditis leads to inflammatory and necrotic lesions in the myocardium 7-10 days after virus inoculation. The purpose of this study was to determine whether hemodynamic changes occur in murine coxsackievirus B 3 myocarditis and whether they are correlated to histological cardiac lesions throughout the infection. Left ventricular function was determined by open chest puncture of the left ventricle in the course of acute coxsackievirus B 3 infection. Histological cross sections of the heart were stained with hematoxylin/eosin and scored blindly for myocarditic lesions. Left ventricular function was preserved until day 7 post-virus inoculation Left ventricular systolic pressure, +dP/dtmax and -dP/dtmax and heart rate declined significantly from day 7 to day 10. The decrease in these parameters did not correlate with viral concentrations in the heart on the day of hemodynamic measurements. The decrease was related to histological changes on day 10, but not on day 7 of the infection. The data suggest (a) that a cumulative loss of cardiac myofibers, induced either by the virus and/or by immune reactions to the heart, is likely to lead to a late depression of cardiac function, and (b) that there is a weak and only temporary structure-function relationship in the heart in coxsackievirus B 3 myocarditis. Therefore, in addition to an analysis of histological changes, the measurement of cardiac function appears to be very important in order to completely evaluate the severity of myocarditis and the usefulness of any therapy.
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PMID:Left ventricular hemodynamic parameters in the course of acute experimental coxsackievirus B 3 myocarditis. 852 20

In mice, depression of hepatic uroporphyrinogen decarboxylase (UROD) leading to porphyrin accumulation (uroporphyria) occurs with chlorinated ligands of the aryl hydrocarbon (AH) receptor especially after iron overload. However, in the absence of chlorinated ligands, iron itself will eventually cause uroporphyria, but this response is not associated with the Ahr genotype. These effects are potentiated by administration of the haem precursor 5-aminolaevulinate (ALA). The aim of this study was to investigate the effects of ALA alone. Prolonged administration of 2 mg ALA/mL in the drinking water to SWR mice also led to decarboxylase insufficiency (11% of control) and uroporphyria by 8 weeks, whereas DBA/2 mice did not show reduced enzyme activity. Both strains are considered AH nonresponsive and analysis of the Ahr gene using restriction fragment length polymorphism was consistent with SWR, like DBA/2, possessing the Ahrd allele. Exposure of isolated hepatocytes to ALA (150-500 microM) for up to 48 hr showed a significant accumulation of both uroporphyrin and coproporphyrin in the medium, which for uroporphyrin particularly was significantly greater with SWR than with DBA/2 cells. Basal in vivo CYP1A2 activity, measured as microsomal methoxyresorufin dealkylation, was significantly greater in SWR than in DBA/2 mice (1.3-fold), but it was unclear whether this was sufficient to explain the marked difference in sensitivities of the two strains. Despite SWR mice being AH nonresponsive, uroporphyria and decarboxylase depression after an initial iron overload and ALA for 3 weeks were greatly potentiated by a single dose (100 mg/kg) of hexachlorobenzene (a weak AH ligand). The results demonstrate that there is a genetic difference in mice independent of the Ahr genotype and response to iron, which influences the susceptibility to ALA-induced uroporphyria. Thus chemicals, iron and ALA can act independently, but also together, to cause porphyria in susceptible individuals.
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PMID:Uroporphyria induced by 5-aminolaevulinic acid alone in Ahrd SWR mice. 893 51

The objective of the present study was to determine the neurobehavioral effects of the putative endogenous cannabinoid ligand, anandamide, and its influence on cannabinoid (CB1) receptor gene expression. The effect of acute administration of anandamide to C57BL/6, DBA/2, and ICR mice were evaluated in motor function and emotionality tests. The C57BL/6 and ICR mouse strains were more sensitive than the DBA/2 strain to the depression of locomotor activity and stereotyped behavior caused by anandamide. Although anandamide produced catalepsy in all three strains, anandamide induced ataxia in the minus-maze test only in the C57BL/6 animals and only at the lowest dose used. In the plus-maze test system, anandamide produced a mild aversive response, and by the third day of treatment the mouse strains developed an intense aversion to the open arms of the plus-maze. Northern analysis data using the recently cloned mouse cannabinoid receptor cDNA as a probe indicated that there was abundant expression of CB1 gene in the whole brain of the ICR mouse than in the brains of the C57BL/6 and DBA/2 strains with or without pretreatment with anandamide. The anandamide induced neurobehavioral profile does not seem to correspond to the CB1 gene expression in the mouse strains. It is, therefore, unlikely that the CB1 receptor mediates all the cannabinomimetic effects of anandamide in the brain.
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PMID:Neurobehavioral effects of anandamide and cannabinoid receptor gene expression in mice. 943 4

FAST and SLOW selected mouse lines were bred for differences in locomotor response to low-dose ethanol. FAST mice exhibit an extreme stimulant response and SLOW mice exhibit locomotor depression at the same ethanol dose. We tested the hypothesis that gamma-aminobutyric acid (GABA) systems modulate ethanol's stimulant effects by examining convulsant responses to GABAA receptor ligands, and by assessing the effects of GABAA and GABAB ligands on locomotor activity in the presence and absence of EtOH. FAST mice were more sensitive to the convulsant effects of GABAA drugs, and to one of two non-GABAergic drugs also tested. FAST and SLOW mice differed in locomotor responses to two benzodiazepines, but not to other GABAA receptor ligands. Ethanol's stimulant effects were not selectively altered by bicuculline or picrotoxin. The selected lines differed in sensitivity to the locomotor depressant effects of the GABAB agonist, baclofen. Ethanol-stimulated activity of FAST mice was inhibited by baclofen, and this effect was reversed by administration of the GABAB antagonist, CGP-35348. These GABAB receptor mediated effects were replicated in DBA/2J inbred mice that exhibit extreme sensitivity to ethanol's stimulant effects. In summary, we found moderate to strong evidence that some sites on the GABAA receptor complex were altered as a consequence of selection of FAST and SLOW mice, but found little support for GABAA mediation of EtOH-stimulated activity. In contrast, we found moderate evidence for differential alteration of GABAB receptor function; however, GABAB receptor involvement in ethanol-stimulated activity was strongly supported by results in the selected lines and an inbred strain.
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PMID:Seizure sensitivity and GABAergic modulation of ethanol sensitivity in selectively bred FAST and SLOW mouse lines. 980 87

Transgenic and knockout mice are used extensively to elucidate the molecular mechanisms of hippocampal synaptic plasticity. However, genetic and phenotypic variations between inbred mouse strains that are used to construct genetic models may confound the interpretation of cellular neurophysiological data derived from these models. Using in vitro slice stimulation and recording methods, we compared the membrane biophysical, cellular electrophysiological, and synaptoplastic properties of hippocampal CA1 neurons in four specific strains of inbred mice: C57BL/6J, CBA/J, DBA/2J, and 129/SvEms/J. Hippocampal long-term potentiation (LTP) induced by theta-pattern stimulation, and by repeated multi-burst 100-Hz stimulation at various interburst intervals, was better maintained in area CA1 of slices from BL/6J mice than in slices from CBA and DBA mice. At an interburst interval of 20 s, maintenance of LTP was impaired in CBA and DBA slices, as compared with BL/6J slices. When the interburst interval was reduced to 3 s, induction of LTP was significantly enhanced in129/SvEms slices, but not in DBA and CBA slices. Long-term depression (LTD) was not significantly different between slices from these four strains. For the four strains examined, CA1 pyramidal neurons showed no significant differences in spike-frequency accommodation, membrane input resistance, and number of spikes elicited by current injection. Synaptically-evoked glutamatergic postsynaptic currents did not significantly differ among CA1 pyramidal neurons in these four strains. Since the observed LTP deficits resembled those previously seen in transgenic mice with reduced hippocampal cAMP-dependent protein kinase (PKA) activity, we searched for possible strain-dependent differences in cAMP-dependent synaptic facilitation induced by forskolin (an activator of adenylate cyclase) and IBMX (a phosphodiesterase inhibitor). We found that forskolin/IBMX-induced synaptic facilitation was deficient in area CA1 of DBA/2J and CBA/J slices, but not in BL/6J and 129/SvEms/J slices. These defects in cAMP-induced synaptic facilitation may underlie the deficits in memory, observed in CBA/J and DBA/2J mice, that have been previously reported. We conclude that hippocampal LTP is influenced by genetic background and by the temporal characteristics of the stimulation protocol. The plasticity of hippocampal synapses in some inbred mouse strains may be "tuned" to particular temporal patterns of synaptic activity. From a broader perspective, our data support the notion that strain-dependent variation in genetic background is an important factor that can influence the synaptoplastic phenotypes observed in studies that use genetically modified mice to explore the molecular bases of synaptic plasticity.
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PMID:Differential maintenance and frequency-dependent tuning of LTP at hippocampal synapses of specific strains of inbred mice. 1106 91


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