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Cocaine self-administration in pigeons.

P J Winsauer1, D M Thompson

  • 1Department of Pharmacology, Medical Center, Georgetown University, Washington, DC 20007.

Pharmacology, Biochemistry, and Behavior
|September 1, 1991
PubMed
Summary
This summary is machine-generated.

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Pigeons self-administered cocaine, demonstrating its reinforcing effects on behavior. Haloperidol, a drug, reduced this cocaine-seeking behavior, suggesting a potential therapeutic target for addiction.

Area of Science:

  • Behavioral Neuroscience
  • Pharmacology
  • Animal Models of Addiction

Background:

  • Cocaine is a potent psychostimulant with high abuse potential.
  • Understanding the neurobiological mechanisms of cocaine self-administration is crucial for developing effective treatments for addiction.

Purpose of the Study:

  • To investigate cocaine's reinforcing properties in pigeons using a multiple schedule of reinforcement.
  • To examine the effects of haloperidol, a dopamine receptor antagonist, on cocaine self-administration behavior.

Main Methods:

  • Pigeons were trained to respond under a multiple schedule where lever presses produced either food or intravenous cocaine infusions.
  • Dose-response effects of cocaine and the impact of saline substitution were assessed.
  • The effects of haloperidol pretreatment on both food- and cocaine-maintained responding were evaluated.

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Main Results:

  • Cocaine maintained responding in a dose-dependent manner, indicating its reinforcing efficacy.
  • Haloperidol administration dose-dependently decreased cocaine self-administration while minimally affecting food-maintained responding.
  • Saline substitution for cocaine led to a decrease in responding, confirming cocaine's role as a reinforcer.

Conclusions:

  • Cocaine acts as a powerful reinforcer in pigeons, supporting self-administration behavior.
  • Haloperidol exhibits antagonist properties against cocaine reinforcement, suggesting the involvement of dopamine pathways in cocaine addiction.
  • Pigeons serve as a valuable model for studying the neuropharmacology of stimulant addiction.