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S C Maxson

Publications and source records attributed to S C Maxson.

At least 37 records · Page 2Linked to original sources
PubMed1985

The role of postnatal testosterone in the development of sexually dimorphic behaviors in DBA/1Bg mice.

The DBA/1 Y chromosome causes an increment in aggression and pubertal testosterone levels. The purpose of the following experiments was to determine whether pubertal testosterone is necessary for the normal development of both aggression and copulation in males. If it is, then the effect of the DBA/1 Y chromosome may be mediated by its influence on pubertal testosterone. Individuals were either castrated at 30 days of age (CAS30) or sham operated (Sham or CAS50). At 50 days of age, the CAS30 individuals were sham operated and replaced with testosterone, while the CAS50 group was castrated and replaced with the same quantity of testosterone. The shams were sham operated at 50 days of age. CAS30 individuals were less aggressive than the CAS50 group, while they were no less aggressive than the sham operated group. Additionally, no groups differed in male copulatory behaviors. The results are discussed in relation to Y chromosomal and developmental mechanisms of sexually dimorphic behaviors.

Age Factors↗
PubMed1984

The DBA/1Bg and DBA/2Bg Y chromosomes compared for their effects on male sexual behavior.

Mount, intromission, and ejaculation number and latency were measured in male mice of the DBA/1Bg, DBA/2Bg, and DBA/2.DBA/1-YBg congenic strains. The DBA/2 and DBA/2.DBA/1-Y congenic strains differ in the source of their Y chromosome. Fifty percent of the DBA/2 and 13 percent of the DBA/2.DBA/1-Y males mounted at least once in the test of male copulatory behavior. There were no other significant differences between these two congenic strains. This finding suggests that the Y chromosome has an effect on the proportion of mice that mount in this test.

Animals↗
PubMed1983

The genetics of hormonal influences on male sexual behavior of mice and rats.

This review focuses on the intersection of genes and hormones as they relate to the development of male sexual behavior. Three major hypotheses are discussed: (1) Some differences in adult male sexual behavior are due to gene differences that influence brain differentiation. Genes that influence brain differentiation may do so by affecting the elaboration of testosterone (i.e., H-Y antigen) or the sensitivity to testosterone (i.e., Tfm mutation and autosomal variations) during neonatal and/or prenatal life. (2) Some differences in male sexual behavior are due to gene differences that influence adult levels of testosterone or sensitivity to testosterone and its metabolites. (3) There is a gene(s) on the Y chromosome that influences the development of sexual behavior that is associated with the arousal mechanism. A possible hormonal mechanism of this Y chromosomal gene(s) is discussed.

Androgen-Insensitivity Syndrome↗
PubMed1983

A mutant for spontaneous seizures in C57BL/10Bg mice.

The symptomatology, electroencephalographic and other correlates, development, and genetics of a new mutant in mice for spontaneous seizures are described. This recessive mutant is designated "spontaneous seizures" and is assigned the gene symbol sps. Just at or after puberty, 25% of the sps/sps homozygotes show behavioral arrest and spontaneous generalized convulsions. The behavioral arrest is associated with 1-2/s high-voltage spikes in the neocortex and the generalized convulsions are associated with paroxysmal activity in the neocortex. The effects of this mutant are compared with those of others for reflex or spontaneous seizures in mice.

Animals↗
PubMed1982

Audiogenic seizure susceptibility of C57BL/6 in equilibrium DBA/2 allophenic mice.

Allophenic mice composed of cells from a strain (DBA/2) susceptible to sound-induced seizures and cells from a strain (C57BL/6) resistant to them were produced by embryo aggregation techniques. Twenty-eight allophenic mice were tested for audiogenic seizure susceptibility. The results were compared with the genotypic composition of the coat melanocytes. For those animals with a predominance of one genotype or the other in the coat, their seizure phenotype was the same as that of the strain most represented in the coat. In contrast, those animals with major contributions of both genotypes in the coat demonstrated the entire spectrum of susceptibility phenotypes. Such results are likely to be a manifestation of a relatively small target tissue for the genes influencing the development of audiogenic seizure susceptibility.

Acoustic Stimulation↗
PubMed1981

Interaction of genotype and fostering in the development of behavior of DBA and C57 mice.

Effects of fostering on behavior were studied in DBA/1Bg and C57BL/10Bg mice. Two-day-old pups were either infostered to mothers of their own strain, crossfostered to mothers of the other strain, or left as controls with their own mothers. Body weight, latency of emergence into an open field, open-field activity, defecation in an open field, spontaneous alternation, passive avoidance learning, and active escape learning were measured when the mice were 22 and 43 days old. Strain differences were observed for each trait except for spontaneous alternation. Fostering per se affected open-field activity and active escape learning. Similar effects of fostering per se on aggressive behavior have been reported by others. These may involve a role of ovarian cytoplasm, X-chromosomal genes, or uterine environment.

Animal Husbandry↗
PubMed1981

Y-chromosome length in sublines of two mouse strains.

Differences in intermale aggression have been repeatedly reported for DBA/1 and C57BL/10 mice. The results of rreciprocal crosses combined with cross-fostering procedures suggest an involvement of the Y chromosome. In the present study, the length of the Y chromosome relative to that of chromosome 19 was ascertained in five sublines of DBA/1Bg, three sublines of C57BL/10Bg, and C57BL/10.DBA/1-Y congenic stock of mice, which carries the DBA/1Bg Y chromosome. With respect to the length of the Y chromosome relative to that of chromosome of 19, two of the DBA/1 sublines are shorter than the other three DBA/1 sublines, and all DBA/1 sublines are shorter than the three C57BL/10 sublines. This is attributable primarily to the length of the Y chromosome. The C57BL/10 sublines and the BL10.D1-Y congenic stock tested exhibit the same relative lengths of the Y chromosome, suggesting that its length has changed on the C57BL/10 genetic background. There is a parallel dependence on autosomal background of the effect of the Y chromosome on intermale aggression.

Aggression↗
PubMed1980

Febrile convulsions in inbred strains of mice susceptible and resistant to audiogenic seizures.

The incidence of febrile convulsions was determined in six inbred strains of mice at four ages. Febrile convulsions were elicited by placing the mice in a cylinder with the air temperature raised to 51 +/- 2 degrees C; this elevated the mouse's body and brain temperature to between 40 and 46 degrees C. The strains used were DBA/2Bg, DBA/1Bg, DBA/1Bg-ras, C57BL/10Bg, C57BL/6Bg, and C57BL/6Bg-Gad-1 alpha; the ages were 21 +/- 1, 29 +/- 1, 59 +/- 1, and 119 +/- 1 days of age. DBA/2Bg, DBA/1Bg, and C57BL/6Bg-Gad 1 alpha are audiogenic seizure susceptible at 21 +/- 1 and 29 +/- 1 days of age, but not at 59 +/- 1 and 119 +/- 1 days of age; whereas C57BL/10Bg, C57BL/6Bg, and DBA/1Bg-ras are audiogenic seizure resistant at all ages. Mice of both sexes, all strains, and all ages had a febrile convulsion and died. Thus, in inbred mice, there does not appear to be either a genetic or developmental correlation between audiogenic seizures and febrile convulsions. This finding may be contrasted with that in other studies showing a correlation between susceptibility to audiogenic seizures and to either electroshock convulsions or chemoconvulsions. However, there are subtle strain and age variants in susceptibility to febrile convulsions of these mice.

Acoustic Stimulation↗
PubMed1979

Interaction of Y-chromosomal and autosomal gene(s) in the development of intermale aggression in mice.

It has been suggested that the Y chromosome of DBA/1Bg mice makes an incremental contribution to their aggressive behavior and to that of the C57BL/10 female X DBA/1 male F1 hybrids. To test this hypothesis, a congenic stock of C57BL/10 with the DBA/1 Y chromosome was developed by the backcross system of breeding; the stock is designated C57BL/10-Y1. There were no significant differences in aggressive behavior between the congenic C57BL/10 and C57BL/10-Y1. However, the hybrid B10D1 F1 and D1B10-Y1 F1 had identical aggression scores, and both of these were more aggressive than the hybrid D1B10 F1. These findings support the hypothesis that there is an interaction between DBA/1 Y chromosomes and autosomes in the development of intermale aggression of these mice.

Aggression↗
PubMed1977

Glucocorticoids and development of audiogenic seizure susceptibility in DBA/1Bg mice.

Metopyrone, an inhibitor of glucocorticoid synthesis, blocks the development of susceptibility to audiogenic seizures in C57BL/6Bg mice after either acoustic priming at 19 days of age or ethanol withdrawal at 70-80 days of age, whereas it has no effect on the development of genetic susceptibility in DBA/1Bg mice. This suggests that there may be similar developmental mechanisms for effects of acoustic priming and ethanol withdrawal on audiogenic seizure risk, which may be different from that for the genetic susceptibility of DBA/1Bg mice.

Acoustic Stimulation↗
PubMed1977

Effect of cortical spreading depression on audiogenic seizure priming of C57BL/6 mice.

At 19 days of age, C57BL/6Bg mice received KCl-induced cortical spreading depression during which they were acoustically primed by exposure to an initial auditory stimulus. At 28 days of age, the mice were tested for susceptibility to audiogenic seizures. Cortical spreading depression had no effect on acoustic priming of C57BL/6Bg mice and it had been previously reported to have no effect on acoustic priming of SJL/J mice. These findings are discussed in the context of pharmacogenetic differences for the effects of aminooxyacetic acid on acoustic priming of C57BL/6 and SJL/J mice.

Acoustic Stimulation↗
PubMed1977

Pharmacogenetic differences in audiogenic seizure priming of C57BL/6Bg and DBA/1Bg-asr mice.

Susceptibility to audiogenic seizures can be induced in some strains of resistant mice by exposure to an initial auditory stimulus (acoustic priming). Aminooxyacetic acid, hydrazine, glutamic acid, gamma-aminobutyric acid (GABA), cycloheximide, and metyrapone antagonize the acoustic priming of audiogenic seizure susceptibility in C57BL/6Bg mice, whereas only metyrapone attenuates that of DBA/1Bg-asr mice. The strain difference in the effect of AOAA and cycloheximide is correlated with a small, transient fall in level of brain GABA in C57BL/6Bg but not DBA41Bg-asr mice. These findings support our hypothesis that there are at least two neural mechanisms of acoustic priming, each with its own genetic basis and that corticosteroids are required by both mechanisms for the development of primed seizures.

Acoustic Stimulation↗