Biomedical subjects

B C Dudek

Publications and source records attributed to B C Dudek.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Differential activating effects of ethanol in C57BL/6Abg and DBA/2Abg mice.

A characteristic pattern of ETOH-induced locomotor activation in the DBA/2Abg strain (D2), small activation or sedation in the C57BL/6Abg (B6), and an intermediate position of the F1s was found using a between-group design and 1.5 g/kg ETOH. This pattern was consistent for a variety of behavioral indices not previously examined, including distance, rest time, movement speed and length, as well as the traditional horizontal counts. Using a within-subject, multiple day, repeated-testing procedure, the same three genotypes were also assessed after manipulating drug administration order, where ETOH exposure (1.5 g/kg) was on either the first or second test day. Another experiment examined the effect of lighting level on the response to 1.5 g/kg ETOH using a within-subjects approach. Neither the testing order nor lighting condition had any major influence on the magnitude of activation as measured by locomotor activity (distance). The pattern of additive genotypic influences exhibited by the B6, D2, and F1 mice is remarkably resistant to these contextual and procedural manipulations.

Animals↗

PubMedDate not supplied

Fetal alcohol effects in long- and short-sleep mice: activity, passive avoidance, and in utero ethanol levels.

Genetic differences in susceptibility to fetal alcohol effects (FAE) have been suggested by both human and animal studies. The Long-Sleep (LS) and Short-Sleep (SS) mouse lines, selectively bred for differences in ethanol-induced narcosis, provide a model for studying differential alcohol sensitivity in the etiology of FAE. LS and SS mice were intubated with either 2.9 g/kg (20% w/v) ethanol (E) or an isocaloric amount of sucrose (S) twice per day (6 hr apart) on Days 7 through 15 of pregnancy. An untreated control group (C) was maintained for each line. Offspring were fostered to lactating Rockland-Swiss mice at birth. LS offspring prenatally exposed to ethanol exhibited increased open-field activity relative to LS controls, but this effect was due to the overactivity of one litter. Activity for SS mice prenatally exposed to ethanol did not differ from control levels. Ethanol content in blood (280 mg/dl), amniotic fluid (258 mg/dl), and fetal tissue (230 mg/dl) did not differ in similarly treated LS and SS dams. In a second experiment, females were treated from Days 7 through 18 of gestation, and their offspring were tested for either open-field activity or passive avoidance learning. There were no group differences in open-field activity, but LS mice prenatally exposed to alcohol took more trials to reach a passive avoidance criterion than their controls, whereas similarly treated SS mice did not differ from controls. These results suggest that genetically-mediated sensitivity to ethanol influences susceptibility to FAE and that this may be task specific.

Animals↗

PubMedDate not supplied

The relationship between ethanol-induced locomotor activation and narcosis in long-sleep and short-sleep mice.

Mice selectively bred for marked response to hypnotic doses of ethanol (long-sleep, LS) respond to subhypnotic doses of ethanol (ETOH) with less stimulation of locomotor activity than their short-sleep (SS) counterparts. This assessment was made by comparing ETOH-induced alterations in locomotor activity to an untreated baseline within individual subjects, and to a saline-treated control group. A correlational study, using the same method in F2 generation hybrids of the LS and SS lines, produced a negative correlation (-.36) between locomotor stimulant effects of a subhypnotic dose of ETOH and length of loss of the righting reflex following a hypnotic dose. This relationship also appeared in a factor analysis of baseline locomotor activity, ETOH-stimulated activity, and depressant response variables. The genetic selection for LS and SS mice appears to have differentiated loci that influence more than one type of behavioral response to ETOH, an example of pleiotropism.

Animals↗