Drug-activation of brain reward pathways.

  title={Drug-activation of brain reward pathways.},
  author={Roy A Wise},
  journal={Drug and alcohol dependence},
  volume={51 1-2},
  • R. Wise
  • Published 1 June 1998
  • Biology, Psychology
  • Drug and alcohol dependence

The Sensitivity of the Crayfish Reward System to Mammalian Drugs of Abuse

This work demonstrates the potential of crayfish as a model system for research into the neural mechanisms of addiction, by contributing an evolutionary, comparative context to the understanding of natural reward as an important life-sustaining process.

Neuronal Nicotinic Acetylcholine Receptors in Reward and Addiction

In this chapter, the expression and function of nAChRs in the reinforcing/rewarding properties of drugs of abuse are explored.

Cannabinoid Regulation of Brain Reward Processing with an Emphasis on the Role of CB1 Receptors: A Step Back into the Future

A comprehensive picture of the current status of what is known about the endocannabinoid system mechanisms that underlie modification of brain-reward processes is provided to provide the development of potential pharmacotherapies designed to treat reward-dysfunction-related disorders.

The Extent of Neuroadaptive Responses to Psychostimulants: Focus on Brain Angiotensin System

The evidence presented in this chapter highlight the RAS as a neuromodulatory system of superior brain activities, and validate Angiotensin II involvement in amphetamine-induced alterations through AT1 receptor activation, which would be prominent candidates for pharmacological treatment in pathologies related to altered dopamine neurotransmission.


Overall, intracranial place conditioning studies showed that there are a number of receptors, neuronal pathways and discrete central nervous system sites involved in the morphine reward mechanisms.

Neuronal Nicotinic Acetylcholine Receptors:Molecular Targets for Alcoholism andEthanol Reward: A Dissertation

It is shown, for the first time, that a specific nAChR subtype, those that contain the α4 subunit (α4*), mediate voluntary ethanol consumption and reward and further supports the hypothesis that α4* nA ChRs are molecular targets for alcohol cessation therapies.

The Mesolimbic Dopamine Reward Circuit in Depression

Impulse activity of midbrain dopamine neurons modulates drug-seeking behavior

Results show that inhibiting dopamine cell impulse activity, by activation of dopamine autoreceptors, reduces drug-seeking behavior, which suggests that the impulse activity of midbrain dopamine cells could be an important factor contributing to relapse.



Opiate reward: Sites and substrates

  • R. Wise
  • Biology, Psychology
    Neuroscience & Biobehavioral Reviews
  • 1989

Brain dopamine and reward.

While the evidence is strong that dopamine plays some fundamental and special role in the rewarding effects of brain stimulation, psychomotor stimulants, opiates, and food, the exact nature of that

Evidence that mesolimbic dopaminergic activation underlies the locomotor stimulant action of nicotine in rats.

In rats which have been chronically treated with l-nicotine, a selective activation of mesolimbic dopamine appears to mediate the locomotor stimulant effect of this drug.

Brain reward circuitry: A case for separate systems

  • A. Phillips
  • Psychology, Biology
    Brain Research Bulletin
  • 1984

Brain reward circuitry: Four circuit elements “wired” in apparent series

Blockade of the reward‐potentiating effects of nicotine on lateral hypothalamic brain stimulation by chlorisondamine

Evidence is added that the direct, endogenous cholinergic contribution to brain stimulation reward is muscarinic and fit with other evidence that the potentiation ofbrain stimulation reward by exogenous nicotine involves actions on nicotinic receptors native to dopaminergic neurons.

Behavioral methods for inferring anatomical linkage between rewarding brain stimulation sites.

It is concluded that self-stimulation of the medial forebrain bundle involves the direct activation of long-axon, longitudinal pathways, and the conduction velocity in the fibers subserving the collision-like effects are consistent with the properties of small myelinated axons but not central monoaminergic fibers.

Rewarding brain stimulation: role of tegmental cholinergic neurons that activate dopamine neurons.

A mechanism for the involvement of Ch5 neurons in drug rewards and antimuscarinic psychosis is proposed and suggests that both acted through the same receptors near Ch5 cells.

Toward a cellular analysis of intracranial self-stimulation: Contributions of collision studies

  • P. Shizgal
  • Biology, Psychology
    Neuroscience & Biobehavioral Reviews
  • 1989