Strain differences in testicular weight and spermatogenesis with special reference to C57BL-10J and DBA-2J mice.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
This study was designed to assess the possible genetic determinants of neurosensitivity to early (neonatal) phenobarbital (PhB) administration and to conduct a strain comparison for the cerebellar histology of both inbred and outbred mice. HS/Ibg, C57BL/10 and DBA/1 pups were injected with 50 mg PhB/kg daily on neonatal days 2-21. On day 50, treated animals (B) of all strains had smaller brains than controls (C). Moreover, the cerebellar area was decreased in HS and C57 B mice but not in DBA mice, suggesting genotype-environment interaction. B mice from all strains had similar Purkinje cell losses. Strain comparison showed that control C57 mice had smaller brains than control HS, and DBA had smaller brains than both HS and C57. Similarly, C57 had smaller cerebellar layers than HS and DBA had smaller cerebellar layers than both HS and C57. DBA and C57 mice had fewer Purkinje cells than HS but did not differ from each other.
Explore the source record for details and available documents.
During development the C57BL/6 and DBA/2 mouse strains present morphological variations in cholinergic forebrain structures correlated with different behavioral reactivities to cholinergic agents. The present research assessed that these strain-dependent differences are also present in cholinergic-mediated analgesia. The administration of oxotremorine (0.0025, 0.005 and 0.01 mg/kg) to 30- and 60-day-old C57 and DBA mice resulted in dose- age- and strain-dependent analgesia. In particular oxotremorine is more effective in DBA/2 than in C57BL/6 mice and the latter strain showed a significant decrease of analgesic response in adulthood.
The effects of lingual treatment with amiloride, an inhibitor of salt taste responses in several mammalian species, on NaCl responses of the chorda tympani nerve were compared between four inbred strains of mouse (BALB/cCrSlc, DBA/2CrSlc, C57BL/6CrSlc and C3H/HeSlc). In C57BL and C3H mice amiloride significantly suppressed responses of the chorda tympani nerve to NaCl at a concentration 0.1 M or more whereas in BALB and DBA mice the drug did not significantly affect the responses to NaCl at any concentration, suggesting a lack of the amiloride-sensitive receptor component for NaCl in the latter two strains. A two-bottle preference test demonstrated that all strains of mouse usually showed no preference for NaCl at any concentration and avoided NaCl at 0.3 M or more, although some differences were observed in that C57BL and C3H mice showed aversive responses to 0.1 and 0.15 M NaCl, whereas BALB and DBA mice were indifferent to these solutions. The results suggest that there exist prominent differences between mouse strains in the amiloride-sensitive component of their salt receptor systems. However, in mice the taste information derived from the amiloride-sensitive receptor component probably has no remarkable effect on behavioral responses to NaCl except for a possible contribution to decreasing aversion thresholds for NaCl by increasing overall taste information about NaCl.
In order to investigate the effects of social isolation on aggressive behavior and GABA levels in different brain areas, inbred mice of the C57 Bl/6 and the DBA/2 strains were housed individually over a period of 8 weeks. Social isolation induced a clear increase of aggressive responses only in the DBA/2 strain and a decrease of GABA levels in septum, striatum, olfactory bulb and posterior colliculus in both the C57Bl/6 and in the DBA/2 strains. An increase of neurotransmitter concentration was observed in amygdala of DBA mice. DBA mice when compared to C57 mice showed significantly lower levels of GABA in olfactory bulb and striatum. These results are discussed in light of several previous studies which have pointed out a correlation between a deficiency of GABA mediated inhibition in some brain areas and different kinds of aggressive behavior as well as the possibility of a blockade of aggressive behavior by potentiation of GABAergic mediated inhibition. A possible suggestion emerging from our results is that the aggressive responses exhibited by isolated DBA mice but not by isolated C57 mice may be related to lower levels of the inhibitory neurotransmitter in the olfactory bulb and striatum.
Explore the source record for details and available documents.
C57BL/6J mice, not susceptible to audiogenic seizures (AGS) on the 1st exposure to an acoustic stimulus, were exposed to the acoustic stimulus for 1 min and then tested at some later date (acoustic priming). They were first exposed at either 8, 16, 19, 22, or 28 days of age, and then tested for AGS 2-16 days after priming. DBA/2J mice, susceptible to AGS on the 1st exposure to intense noise, were exposed to the acoustic stimulus at 26 days of age, and then again 2-14 days later. Data indicate that the incidence of AGS upon the 2nd exposure to the acoustic stimulus is a function of age at priming, the prime-to-test interval in days, and the index of seizures. In the case of DBA mice, later effects are also dependent on the initial level of seizure.
AB/Jena, DBA/2Jena, C57B1/6 Jena inbred mice and ABD2F1- and B6D2F4-hybrid mice either were reared communally and weaned at day 30 or were reared by isolated mothers and weaned at day 21 (I21). On day 50 the total RNA content of pyramidal brain cells of male offspring was determined by cytophotometry. The studied brain areas were the frontal pole of cerebral cortex (FCC) and the CA1 region of the dorsal hippocampus (DHI). The DBA, C57 and ABD2 mice had a reduced FCC and DHI RNA-content under I21-rearing. Under these conditions the AB strain has the highest RNA-content in both substrates. The results call for the awareness of possible genetic influences when studying the effects of environmental enrichment/impoverishing.
Ethanol is metabolized in human and rodent liver primarily by the enzyme alcohol dehydrogenase (ADH). Hepatic ADH activity in adult males and females of seven inbred strains of mice was determined to examine genotype- and sex-dependent variability among the strains and the level of sexual dimorphism in each of the strains. ADH activity varied considerably among the strains, which could be categorized into high-activity strains C57BL/6, C57Brcd, and Swiss, and relatively low-activity strains C3H, CBA, and DBA. Adult Swiss, AKR, C57BL/6, and DBA females exhibited significantly higher levels of hepatic ADH than their male counterparts, whereas no gender differences were seen in C3H, CBA, and C57Brcd. Young mice of high and/or low ADH activity strains viz. C57BL/6 and C3H did not exhibit gender differences in ADH activity at weanling but the enzyme levels increased by sixth week in females and remained higher thereafter. The progeny of a high-activity strain with sexual dimorphism (C57BL/6) and a low-activity strain lacking gender difference (C3H) exhibited intermediate levels of ADH and age-dependent sexual dimorphism.
Testicular and Leydig cell function were studied in four inbred strains of mice. Significant strain-related differences were found in the number of LH receptors and in the production of testosterone in vitro in response to increasing concentrations of human CG (hCG) by both decapsulated testes and isolated Leydig cells. Maximal testicular testosterone production was similar in the C57BL/10J and C57BL/6J strains and considerably less in the DBA/2J (DBA) and C3H/HeJ strains, which were similar. However, the number of testicular LH receptors was less in C57BL/6J mice than in all three other strains. The pattern of maximal testosterone production by isolated Leydig cells among the four strains was similar to that observed for whole testes, whereas the number of LH receptors per 10(6) Leydig cells was least for Leydig cells from the DBA strain. When the number of Leydig cells per testis was estimated by dividing the number of testicular LH receptors by the number of LH receptors in 10(6) Leydig cells, it was apparent that testes from DBA mice contain approximately twice as many Leydig cells as those from the other strains. Differences in maximal testicular testosterone production appear to be reflected in differences in maximal testosterone production by isolated Leydig cells from each strain. However, there were no differences in testicular sensitivity to hCG but there were differences in Leydig cell sensitivity to hCG among the four strains. Furthermore, the existence of strain-related differences in well defined functional characteristics of Leydig cells offers the opportunity to study the genetic as well as physiological mechanisms involved in the regulation of Leydig cell function in normal individuals.
The C57BLKS/J (BKS) inbred mouse strain is a widely used animal model of type 2 diabetes. In the presence of the diabetes (db) mutation, obese BKS-db mice develop severe diabetes. Genetic studies of diabetes-susceptibility in this strain are facilitated by the fact that BKS is a genetic composite between the diabetes-resistant C57BL/6J (B6) and susceptible DBA/2J (DBA) strains. On this basis, it has been hypothesized that diabetes-susceptibility in BKS is conferred by DBA-derived alleles. However, recent studies revealed non-B6/non-DBA genetic material in BKS. To identify the origin of this genetic component, we generated a genomic map of BKS using 537 microsatellite markers. Our results demonstrate that, in addition to B6 and DBA, BKS contains alleles from at least three other strains, including 129, C57BL/10 and an unidentified mouse strain. We also analyzed two congenic strains, B6-db and BKS-db, which are widely used for the genetic mapping of diabetes-susceptibility loci. We identified several donor-derived genomic regions introduced during the generation of these congenic strains. In summary, our study reveals novel aspects of the genetic fine-structure of BKS and related strains and facilitates the identification of diabetes-susceptibility loci in this mouse model.
Explore the source record for details and available documents.
Differences in the midsagittal area of the corpus callosum have been reported between human males and females, between handled and nonhandled rats, and both within and between various strains of mice. This measure has, in addition, been related to handedness in humans and "pawedness" in certain strains of mice. The present study investigated the between- and within-strain differences in three inbred strains of mice, two with autoimmune disorders and spontaneously occurring developmental neuropathology, in the midsagittal area of the corpus callosum, the total neocortical volume, and the asymmetry of the neocortex. These morphometric measures were obtained from coronally sectioned celloidin-embedded material from New Zealand Black (NZB/BINJ), BXSB/MpJ, and DBA/2J mouse strains. NZB mice had a total neocortical volume larger than that of either the BXSB or DBA strains, whereas the BSXB mice had a midsagittal area of the corpus callosum larger than that of either of the other two strains. In addition, there was a positive correlation between these two measures. There was no correlation between total neocortical asymmetry and midsagittal area of the corpus callosum in any of the three strains. Finally, there were no differences in any morphometric measure between animals with or without developmental neuropathology in any given strain.
Using a stereological method, the optical disector, we examined three inbred strains of mice (NZB/BINJ, DBA/2, and C57BL/6J) for morphological differences in volume, neuronal number, and density of the pyramidal cell and dentate gyrus granule cell layers of the hippocampus. We found significant differences in volume and neuronal number for both regions between the three strains at 9 weeks of age, but only modest differences in neuronal density. The left dentate volume was 90% larger in the NZB strain and 70% greater in the DBA strain (P<0.0001), and the left pyramidal cell layer was 144% larger in the NZB strain and 150% larger in the DBA strain, than in the B6 strain (P<0.0001). Neuron number in the left dentate was 81% greater in NZB and 37% greater in DBA (P<0.001), and in the left pyramidal cell layer 118% greater in the NZB and 92% greater in the DBA (P<0.01). Differences in neuronal density of the left dentate were not significant (P = 0.060, ns). For the left pyramidal cell layer, neuronal density was 14% greater in B6 and 34% greater in NZB than the DBA strain (P = 0.016). No significant differences were found in left-right laterality, or according to sex. We found that strain accounted for 60% of the variance in hippocampal volume and 44% of neuron number. These differences thus mainly reflect genetic variation in hippocampal volume and may have important implications for brain evolution, behaviour, and human diseases where hippocampal degeneration is involved.
A mouse monoclonal antibody (IgM) was obtained by cell hybridization between X63-Ag8.653 myeloma cells and spleen cells from a BALB mouse that was immunized with GRSL leukemia cells of the GR strain. This antibody identified a unique fetal antigen, which is expressed exclusively on embryonic thymocytes of all strains tested. Therefore, the antigen defined was named fetal thymus antigen-1, FT-1. The proportion of FT-1+ fetal thymocytes detected by immunofluorescence assay sharply decreases as gestation time increases, and finally they disappear from the thymus. On the other hand, Thy-1+ cells increase in inverse proportion. The immunofluorescence studies and absorption tests showed that FT-1 antigen is not detectable on brain, liver, kidney, or lymphoid tissue cells of adult mice. However, it is expressed on some leukemia cells of various mouse strains, which demonstrated that this is the first example of an oncofetal antigen of a mouse leukemia. The molecular weight of FT-1 antigen on leukemia cells was estimated to be 130,000 by means of biosynthetic labeling with [3H]galactose and [35S]methionine. The two-dimensional gel electrophoresis pattern of FT-1 antigen shows a family of glycoproteins with extensive charge heterogeneity. It was also shown that the FT-1 antigen molecule carries the receptor for DBA lectin.
Susceptibility to cadmium (Cd) hepatotoxicity differs among inbred strains of mice. For example, C3H/HeJ mice are sensitive to Cd-induced hepatotoxicity, whereas DBA/2J mice are resistant. The mechanism of genetic predisposition to Cd hepatotoxicity is unknown. A contemporary theory for acute target organ intoxication maintains that Cd initially damages vascular endothelium and parenchymal cell injury is a secondary event that results from localized ischemia. In the present study, the hypothesis that hepatic endothelial cells (EC) of C3H mice are more susceptible to Cd toxicity than those of DBA mice was tested. Hepatic parenchymal and endothelial cells were grown separately on monolayer cultures for 22 h and subsequently treated with various concentrations of Cd. Hepatocellular toxicity was assessed by lactate dehydrogenase leakage and intracellular K+ loss, whereas endothelial cell injury was assessed by trypan blue exclusion and the inhibition of protein synthesis. The susceptibility of hepatocytes to the cytotoxic effects of Cd was identical between strains. In contrast, the vulnerability of EC to Cd intoxication was strain-dependent. When exposed to 2.5-10.0 microM Cd, EC of Cd-sensitive mice were more susceptible to the cytotoxic effects of Cd than those of Cd-resistant mice. Basal metallothionein (MT) levels as well as Cd uptake into EC were similar in the two strains. Following Cd exposure, EC of Cd-sensitive mice accumulated similar amounts of MT as EC of Cd-resistant mice. These observations suggest that the microvasculature in livers of inbred mice is the target tissue responsible for strain-dependent susceptibility to Cd-induced liver injury. The mechanisms that account for this genetic variation in endothelial cell response to Cd are unknown, but do not appear to be related to the cellular disposition of Cd nor to a defect in the metabolism of MT.
Newborn male DBA/2 and C57BL/6 mice were either crossfostered, fostered within strains, or, after handling, left with their own dams and compared for nine behavioral compenents observed in single animals at an adult age and for body weight measured at 4 weeks and 3 months. Many strain differences between the unfostered control groups emerged and these remained largely unchanged in comparisons between the infostered and between the outfostered groups. In neither infostered group were significant influences of fostering per se found. Some variation due to foster strain was detected mainly in the DBA outfostered group, namely, for 4-week body weight, rearing frequency, and locomotor activity, but no resemblance to the alien strain was brought about by this. Effects of litter occurred rarely. Unlike the C57BL strain, the DBAs showed a clear pattern of interdependence among exploratory acts. In spite of problems that may be attached to the crossfostering method, it was concluded that postnatal genotype-dependent maternal influences were rather unimportant as a source of variation in behavior and growth as measured between these two strains, relative to direct genetic effects and, possibly, prenatal factors.