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J R Wenger

Publications and source records attributed to J R Wenger.

8 recordsLinked to original sources
PubMed1986

Sodium pentobarbital-induced cross-tolerance to ethanol is learned in the rat.

Initially, rats were trained to walk on a treadmill to avoid footshock. Subsequently, rats given additional practice while pentobarbital-intoxicated became cross-tolerant to ethanol. However, rats given equivalent doses of pentobarbital after practice did not become cross-tolerant, nor did saline-vehicle controls. These results challenge the theories of cross-tolerance which are based exclusively upon cellular adaptations to pharmacological stimulation of drug-responsive neurons. That all of the cross-tolerance measured was attributable to the intoxicated practice suggests that this observed cross-tolerance was mediated by some form of learning.

Animals↗
PubMed1983

Cholecystokinin produces conditioned place-aversions, not place-preferences, in food-deprived rats: evidence against involvement in satiety.

The net reinforcing/aversive properties of cholecystokinin (CCK) were measured using a conditioned place-preference paradigm. Both sated and food-deprived rats showed a dose dependent aversion to an environment previously paired with CCK that was correlated with the effects of CCK on feeding. In contrast, all rats showed a conditioned preference for an environment previously paired with food. These results demonstrate the aversive properties of CCK and suggest that the decrease in feeding that follows peripheral administration of CCK results from a CCK-induced malaise.

Animals↗
PubMed1981

Ethanol tolerance in the rat is learned.

Rats were trained to walk on a treadmill to avoid foot shock. The animals developed tolerance for ethanol if given subsequent practice while ethanol intoxicated. Rats given equivalent doses of ethanol after practice did not develop tolerance, nor did saline-treated controls. These results challenge the hypothesis that mere repeated doses of ethanol are sufficient to induce tolerance. It seems that tolerance does not develop unless the response used to measure tolerance is performed while the subject is intoxicated.

Animals↗
PubMed1978

Vitamin D dependence and aboral gradient of in vivo intestinal calcium transport in the rat.

Rates of small-and large-intestinal calcium transport and their dependence on low doses of vitamin D were compared. Young rats were depleted of vitamin D by feeding a rachito-genic diet for 8--9 weeks; 48 and 24 hr prior to study, half were repleted with 200 IU vitamin D2. Duodenum and ileum, or cecum and colon, were perfused separately in situ with 1.6 mM calcium and tracer 45Ca in saline. There was an aboral gradient for net calcium transport and lumen-to-plasma flux with higher values in proximal than distal segments. Vitamin D repletion increased net calcium flux and lumen-to-plasma flux in duodenum and ileum, but not cecum and colon. Plasma-to-lumen flux (calculated as the difference between lumen-to-plasma flux and net flux) tended to be higher in colon than other segments and was not altered by vitamin D repletion.

Animals↗
PubMedDate not supplied

Temperature dependence of ethanol depression in C57BL/6 and BALB/c mice.

The relationship between environmental temperature, body temperature and brain sensitivity to ethanol was investigated in male C57BL/6S and BALB/cS mice. Age-matched, drug-naive mice of both strains were injected with 3.6 g/kg ethanol (20% w/v) and placed into a chamber kept at one of eight designated temperatures from 12 to 36 degrees C. Chamber temperature significantly affected wake-up rectal temperatures, sleep-times and wake-up brain ethanol concentrations in the intoxicated mice. Wake-up rectal temperatures were significantly, positively correlated with sleep-times and significantly, negatively correlated with wake-up brain ethanol concentrations in both strains. Linear regression analyses indicated that up to 47% of the variability in ethanol sensitivity of C57 mice and up to 31% of the variability in sensitivity of BALB mice could be accounted for by their wake-up rectal temperatures suggesting that the effects of ambient temperature on ethanol sensitivity were mediated, in part, by the resultant body temperatures. These results replicate and extend previous findings and demonstrate that temperature dependence of ethanol depression is not strain specific. The correlational and regression analyses provide additional evidence that brain sensitivity to ethanol depression varies with body temperature in accordance with membrane perturbation theories of anesthesia.

Animals↗