No abstract

Lemon, Christian H., Susan M. Brasser, David V. Smith. Alcohol activates a sucrose-responsive gustatory neural pathway. J Neurophysiol 92: 536 -544, 2004. First published February 25, 2004 10.1152/jn.00097.2004. A strong positive association exists between the ingestion of alcohol and sweet-tasting solutions. The neural mechanisms underlying this relationship are unknown, although recent data suggest that gustatory substrates are involved. Here, we examined the role of sweet taste receptors and central neural circuits for sugar taste in the gustatory processing of ethanol. Taste responses to ethanol (3, 5, 10, 15, 25, and 40% vol/vol) and stimuli of different taste qualities (e.g., sucrose, NaCl, HCl, and quinine-HCl) were recorded from neurons of the nucleus of the solitary tract in anesthetized rats prior to and after oral application of the sweet receptor blocker gurmarin. The magnitude of ethanol-evoked activity was compared between sucroseresponsive (n ϭ 21) and sucrose-unresponsive (n ϭ 20) neurons and the central neural representation of ethanol taste was explored using multivariate analysis. Ethanol produced robust concentration-dependent responses in sucrose-responsive neurons that were dramatically larger than those in sucrose-unresponsive cells. Gurmarin selectively and similarly inhibited ethanol and sucrose responses, leaving NaCl, HCl, and quinine responses unaltered. Across-neuron patterns of response to ethanol were most similar to those evoked by sucrose, becoming increasingly more so as the ethanol concentration was raised. Results implicate taste receptors for sucrose as candidate receptors for ethanol and reveal that alcohol and sugar taste are represented similarly by gustatory activity in the CNS. These findings have important implications for the sensory and reward properties of alcohol.

These results support other clinical and laboratory-based research indicating that persistent heroin use may be reduced by providing larger methadone maintenance doses that produce more effective cross-tolerance to heroin.

This study examined differential responding of juvenile, adolescent, and adult rats after intoxication from an acute alcohol challenge. Experiment I generated blood ethanol curves for subjects 25, 35, or 110 days postnatal, after doses of 2.0 or 4.0 g/kg, assessing elimination rates and time of drug clearance. Experiment 2 compared ethanol's initial hypothermic and delayed hyperthermic effect across age by 48-hr temperature measurement with telemetry. At clearance or 24 hr after alcohol exposure, Experiment 3 tested subjects for changes in acoustic startle reactivity and ultrasonic vocalization (USV). Younger rats showed an absent or reduced tendency for residual hyperthermia, and adults showed alterations in USV observed as aftereffects of intoxication, despite greater initial blood alcohol levels and ethanol hypothermia in the former. The lesser ethanol hangover effects in weanlings and adolescents may be due in part to faster ethanol elimination at these ages compared with adults.

This study tested the hypothesis that increased processing or efficacy of the unconditioned stimulus (US) contributes to the facilitation of trace conditioning that occurs when preweanling rats are conditioned in a novel sensory-rich context. Experiment 1 extended previous findings (D. L. McKinzie & N. E. Spear, 1995) of facilitated acoustic trace conditioning in the 17-day-old rat in a sensory-enhanced versus a home odor context. In the enhanced or more familiar context, Experiment 2 tested rats of this age for degree of spontaneous locomotor activity and ultrasonic vocalizations, activity and ultrasounding in response to shock, and the acoustic startle reflex. The enhanced context resulted in a greater overall activity response to shock, increased ultrasounding to discrete shocks, and a sensitized latency to startle. The results suggest that enhanced US processing in a sensory-rich context is a likely contributor to its facilitative effect on infant learning.