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Animal models of compulsive behavior.

R K Pitman1

  • 1Research Service, Veterans Administration Medical Center, Manchester, NH 03104.

Biological Psychiatry
|June 1, 1989
PubMed
Summary
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Compulsive disorders may stem from basal ganglia or limbic system disturbances. Animal research suggests models involving dopamine excess in the basal ganglia, but human causes may vary.

Area of Science:

  • Neuroscience
  • Behavioral Science

Background:

  • Clinical and pathological evidence implicates the basal ganglia in compulsive disorders.
  • The limbic system may also play a role in the pathophysiology of compulsive behaviors.

Purpose of the Study:

  • To explore how disturbances in the basal ganglia and limbic system may lead to compulsive behavior.
  • To present animal research models explaining the neurobiological underpinnings of compulsive behaviors.

Main Methods:

  • Review of animal research on compulsive behavior.
  • Analysis of potential neurobiological models including reinforcement, striatal function, displacement behavior, and hippocampal modulation.
  • Examination of the role of dopaminergic activity.

Main Results:

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  • Several models are proposed: stimulation of reinforcement, striatal comparator dysfunction, displacement behavior modulation, and hippocampal interference with reward effects.
  • A common feature across these models is an apparent excess of dopaminergic activity in the basal ganglia.

Conclusions:

  • While dopaminergic hyperactivity in the basal ganglia is a common theme, it may not be the sole cause of all human compulsive behaviors.
  • Further research is needed to fully elucidate the complex neurobiology of compulsive disorders.