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Related Experiment Videos

Dextrorphan effects on cocaine and brainstem perturbation

M Lundien1, O J Andy, R W Rockhold

  • 1Dept. of Neurosurgery, U. of Mississippi Med Center, Jackson 39126, USA.

Integrative Physiological and Behavioral Science : the Official Journal of the Pavlovian Society
|July 1, 1996
PubMed
Summary

Dextrorphan, an N-methyl-D-aspartate receptor blocker, reduced hyperactivity in rats. Combined with cocaine, dextrorphan counteracted cocaine

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Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Dextrorphan is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors.
  • NMDA blockers are known to reduce the locomotor stimulatory and toxic effects of cocaine.

Purpose of the Study:

  • To investigate if dextrorphan attenuates cocaine-induced behavioral excitatory motor activity.
  • To evaluate the effects of dextrorphan and brainstem lesions on motor activity and escape behavior.

Main Methods:

  • 25 Spontaneously Hypertensive Rats (SHR) were used, with some receiving cocaine via mini-osmotic pumps.
  • Dextrorphan challenges were administered, with some rats also receiving cocaine.
  • Brainstem lesions and electrode implants were utilized to assess behavioral responses.

Main Results:

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  • Dextrorphan alone reduced motor activity in naive and lesioned rats.
  • Combined cocaine and dextrorphan increased motor activity in naive rats but decreased it in electrode implant subjects.
  • Brainstem lesions attenuated escape behavior and altered various behaviors.

Conclusions:

  • Dextrorphan and brainstem lesions effectively reduced motor hyperactivity and escape behavior.
  • Dextrorphan counteracted the excitatory motor effects of cocaine in electrode implant subjects.
  • Dextrorphan did not induce or facilitate seizures.