The disruptive effects of methamphetamine on delayed-matching-to-sample performance reflect proactive interference

Anne C Macaskill1, Catherine C Harrow1, David N Harper1

  • 1Victoria University of Wellington, School of Psychology, PO Box 600, Wellington, New Zealand.

Insights

Methamphetamine, like MDMA, increases proactive interference in rats, impairing working memory. This effect, linked to dopamine D1 receptor activity, was lessened by a D1 antagonist.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cognitive Psychology

Background:

  • Drugs of abuse, such as MDMA, cause specific cognitive impairments.
  • Proactive interference, a disruption in memory where prior learning hinders new learning, is one such impairment.
  • Stimulant-based drugs may affect working memory through response repetition tendencies.

Purpose of the Study:

  • To investigate if methamphetamine induces proactive interference in rats using a delayed matching-to-sample task.
  • To explore the role of dopamine D1 receptors in methamphetamine-induced cognitive deficits.

Main Methods:

  • Rats were trained on a delayed matching-to-sample task.
  • Methamphetamine's effect on accuracy was assessed, particularly on trials requiring a different response than the previous trial.
  • The impact of the dopamine D1 antagonist SCH23390 on methamphetamine's effects was evaluated.

Main Results:

  • Methamphetamine significantly increased proactive interference, reducing accuracy when a different response was required.
  • This impairment suggests a disruption in working memory similar to that caused by MDMA.
  • Pre-administration of SCH23390 attenuated the proactive interference caused by methamphetamine.

Conclusions:

  • Methamphetamine, a stimulant drug, disrupts working memory by increasing proactive interference in rats.
  • This cognitive disruption is mediated, in part, by dopamine D1 receptor activity.
  • Findings support the hypothesis that stimulant-induced working memory deficits are linked to response repetition and D1 receptor function.