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Adenosine triphosphate blocks opiate withdrawal symptoms in rats and mice

A A Gomaa1, S A Moustafa, A A Farghali

  • 1Department of Pharmacology, Faculty of Medicine, Assiut University, Egypt.

Pharmacology & Toxicology
|January 1, 1989
PubMed

Insights

Adenosine triphosphate (ATP) significantly reduces opiate withdrawal symptoms in animal models. ATP administration effectively blocks jumping behavior and abnormal physiological responses associated with morphine withdrawal.

Area of Science:

  • Pharmacology
  • Neuroscience
  • Physiology

Background:

  • Opiate dependence and withdrawal present significant clinical challenges.
  • Understanding the neurobiological mechanisms of withdrawal is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the anti-withdrawal effects of adenosine triphosphate (ATP).
  • To determine ATP's ability to modify or block key signs of opiate withdrawal.

Main Methods:

  • A chronic morphine-dependence model was used in mice and rats.
  • Adenosine triphosphate (ATP) was administered intravenously.
  • Naloxone was used to precipitate withdrawal symptoms.
  • Measurements included withdrawal jumping, intestinal hypermyoelectric activity, and arterial blood pressure.
  • The role of alpha 2-adrenoreceptors was assessed using yohimbine.

Main Results:

  • ATP significantly increased the naloxone ED50 for withdrawal jumping by 11-fold.
  • ATP (1 and 2 mg/kg) inhibited naloxone-precipitated intestinal hypermyoelectric activity in 80% and 100% of animals, respectively.
  • ATP dose-dependently blocked the increase in mean arterial blood pressure during withdrawal.
  • Yohimbine reversed ATP's effects on intestinal activity but not on jumping or blood pressure changes.

Conclusions:

  • Adenosine triphosphate (ATP) demonstrates significant anti-withdrawal properties against opiate dependence.
  • ATP effectively mitigates key physiological and behavioral manifestations of morphine withdrawal.
  • The anti-withdrawal actions of ATP involve complex mechanisms, partially mediated by alpha 2-adrenoreceptors for gastrointestinal effects.

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