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  • Influence
Oral alcohol self-administration stimulates dopamine release in the rat nucleus accumbens: genetic and motivational determinants.
Dopaminergic neurotransmission in the nucleus accumbens may be an important factor in ethanol reinforcement and genetically determined ethanol preference. This hypothesis was tested by measuringExpand
Control of cocaine-seeking behavior by drug-associated stimuli in rats: effects on recovery of extinguished operant-responding and extracellular dopamine levels in amygdala and nucleus accumbens.
It is demonstrated that cocaine-predictive stimuli elicit robust and persistent cocaine-seeking behavior, and that this effect may involve activation of dopamine transmission in the NAcc and amygdala. Expand
Increase of extracellular corticotropin-releasing factor-like immunoreactivity levels in the amygdala of awake rats during restraint stress and ethanol withdrawal as measured by microdialysis
A progressive increase of CRF-IR levels over time was observed, reaching peak values at 10–12 hr after the onset of withdrawal, and this hypothesis was explored in a series of experiments using intracranial microdialysis to monitorCRF-like immunoreactivity in the extracellular compartment of the rat amygdala. Expand
Cocaine-predictive stimulus induces drug-seeking behavior and neural activation in limbic brain regions after multiple months of abstinence: reversal by D(1) antagonists.
The undiminished efficacy of the cocaine S(D) to elicit drug-seeking behavior after 4 months of abstinence parallels the long-lasting nature of conditioned cue reactivity and cue-induced cocaine craving in humans, and confirms a significant role of learning factors in the long,lasting addictive potential of cocaine. Expand
Ethanol Self-Administration Restores Withdrawal-Associated Deficiencies in Accumbal Dopamine and 5-Hydroxytryptamine Release in Dependent Rats
It is suggested that deficits in accumbal monoamine release may contribute to the negative affective consequences ethanol withdrawal and, thereby, motivate ethanol-seeking behavior in dependent subjects. Expand
Suppression of Ethanol-Reinforced Behavior by Naltrexone Is Associated with Attenuation of the Ethanol-Induced Increase in Dialysate Dopamine Levels in the Nucleus Accumbens
The opiate antagonist naltrexone suppresses ethanol-reinforced behavior in animals and decreases ethanol intake in humans. However, the mechanisms underlying these actions are not well understood.Expand
The dopamine hypothesis of reward: past and current status
Evidence suggests that dopaminergic-neuron activation aids the organism in learning to recognize stimuli associated with internal rewarding or aversive events and long-lasting neuroadaptive changes in mesolimbic dopamine-mediated transmission that develop during chronic drug use might contribute to compulsive drug-seeking behavior and relapse. Expand
Additive Effect of Stress and Drug Cues on Reinstatement of Ethanol Seeking: Exacerbation by History of Dependence and Role of Concurrent Activation of Corticotropin-Releasing Factor and Opioid
  • Xiu Liu, F. Weiss
  • Psychology, Medicine
  • The Journal of Neuroscience
  • 15 September 2002
The results document that stress and drug-related environmental stimuli interact to augment the resumption of drug seeking after extinction and suggest that this effect results from concurrent activation of opioid and CRF transmission. Expand
Neurocircuitry targets in ethanol reward and dependence.
Current work has begun to define the neurocircuits responsible for the two major sources of reinforcement key to animal models of excessive ethanol intake: positive and negative reinforcement. Expand
Animal models of drug craving
The development of animal models of drug craving will have heuristic value and allow a systematic investigation of the neurobiological mechanisms of craving, and these animal models are evaluated according to reliability and predictive validity. Expand