Biomedical subjects
Publications and source records attributed to J Stenger.
Rayleigh scattering off a Bose-Einstein condensate was studied. Exposing an elongated condensate to a single off-resonant laser beam resulted in the observation of highly directional scattering of light and atoms. This collective light scattering is caused by the coherent center-of-mass motion of the atoms in the condensate. A directional beam of recoiling atoms was built up by matter wave amplification.
Considerable evidence indicates a critical role for dopamine in the reinforcing effects of cocaine. Because dopamine has been shown to be a critical modulator of gap junction communication in both eye and brain, we sought to examine whether extended intravenous cocaine self-administration would affect the expression of gap junction channel-forming proteins (connexins). Using ELISA, Western analysis, immunohistochemistry, semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR), and non-radioactive in situ hybridization, we demonstrate that withdrawal from chronic cocaine self-administration causes lasting changes in connexin32 (Cx32) expression in the nucleus accumbens and hippocampus at 2, 7 and 21 days after the last cocaine injection. A sustained decrease in Cx32 protein and mRNA levels is noted in areas that have been implicated in cocaine craving (i.e. nucleus accumbens and subfields of the hippocampal formation). A progressive increase in gap junction protein and mRNA expression is noted in areas that become hyperexcitable after chronic cocaine exposure (i.e. CA1 hippocampal neurons). We speculate that gap junction communication may be critically involved in reinforcement processes and neuroadaptive changes produced by drugs of abuse.
Total body electrical conductivity (TOBEC) predictions of overall body fat were compared to combined perirenal and epididymal fat pad weights. The latter are considered to be reasonable estimates of overall adiposity. TOBEC was used to measure the body composition of 40 male Long-Evans and two male Sprague-Dawley rats ranging in weight from 210-505 g. The animals were then sacrificed and the perirenal and epididymal fat pads were removed and weighed. Core temperature was recorded before and after TOBEC values were collected. To assess the effect of position, two values were obtained for young rats: one when the tail was tucked under the rat's body and another when the tail was extended such that the full length of the measurement chamber was occupied. The TOBEC-predicted body fat was significantly different for these two positions. The best correlation between fat pad weight and TOBEC-predicted body fat (r = 0.83) was obtained when young animals were in the tail-extended position. The reliability of TOBEC readings appears to be reasonably good with mature rats.
This report follows up our earlier finding that chronic ventromedial hypothalamic stimulation caused an inhibition of weight gain. In this study we examined the contribution of stimulation-induced activity and brown adipose tissue thermogenesis to the reduced weight gain following three sessions of low-level stimulation delivered every other day to the ventromedial hypothalamus and adjacent areas. During stimulation trials, activity level was ranked on a dichotomous scale. Weight gain and food intake were subsequently monitored for an additional 4 weeks, after which the effects of a 60-s stimulation trial on the temperature of core and interscapular brown adipose tissue were evaluated. The highest activity was associated with the ventromedial hypothalamic sites and this factor contributed significantly to the difference in weight gain and food intake resulting from stimulation of the ventromedial hypothalamus and other areas. These differences largely disappeared during the follow-up period. With little exception, none of the sites elicited temperature changes in brown adipose tissue. As demonstrated in acute work, the contribution of stimulation-induced activity must be dissociated from the metabolic changes that occur in response to ventromedial hypothalamic stimulation.
The effects of chronic stimulation of the ventromedial hypothalamus and adjacent structures on body weight, food intake, and epididymal fat pad weight were examined in normophagic rats. Three hours of intermittent low level electrical stimulation were delivered three times per week for four weeks; body weight and food intake were monitored for an additional ten days after stimulation trials had ceased. Animals receiving ventromedial hypothalamic stimulation had the shallowest growth curves while stimulation of other structures produced a rate of growth that fell between that of the ventromedial hypothalamic and the implanted control group. This pattern persisted during the poststimulation phase. Food intake, while initially depressed in the stimulated groups, began to approach control levels by the third week of stimulation. Efficiency of food utilization (weight gain/consumption) was significantly reduced during the first week of stimulation in the ventromedial hypothalamic stimulated group. Fat pad weight was slightly decreased in this group as well. These findings suggest that chronic stimulation of the ventromedial hypothalamus causes a persistent shift in metabolic rate that results in a long-term inhibition of weight gain.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.