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Related Experiment Videos

Ketamine blocks the plasticity associated with prefrontal cortex self-stimulation.

D Corbett1

  • 1Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.

Pharmacology, Biochemistry, and Behavior
|December 1, 1990
PubMed
Summary

Noncontingent stimulation of the medial prefrontal cortex (MFC) speeds up intracranial self-stimulation (ICSS) acquisition. This effect is blocked by ketamine, highlighting the role of N-methyl-D-aspartate (NMDA) receptors in neural plasticity.

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Area of Science:

  • Neuroscience
  • Behavioral Neuroscience
  • Neuroplasticity

Background:

  • Intracranial self-stimulation (ICSS) in the medial prefrontal cortex (MFC) is typically acquired slowly.
  • Prior noncontingent stimulation can accelerate ICSS acquisition.
  • N-methyl-D-aspartate (NMDA) receptors are implicated in neural plasticity.

Purpose of the Study:

  • To investigate the role of NMDA receptors in the facilitatory effects of noncontingent MFC stimulation on ICSS acquisition.
  • To determine if NMDA receptor antagonism blocks the acceleration of ICSS.

Main Methods:

  • Rats underwent noncontingent stimulation of MFC ICSS electrodes.
  • Subsequent ICSS acquisition was measured.
  • Ketamine, an NMDA receptor antagonist, was administered prior to noncontingent stimulation in some groups.

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Main Results:

  • Noncontingent MFC stimulation significantly hastened ICSS acquisition.
  • Pretreatment with ketamine blocked the facilitatory effect of noncontingent MFC stimulation on ICSS acquisition.
  • This suggests NMDA receptor involvement in the observed plasticity.

Conclusions:

  • NMDA receptors play a critical role in the neural plasticity underlying the acceleration of ICSS acquisition by noncontingent MFC stimulation.
  • These findings support the involvement of NMDA receptors in experience-dependent changes in neural circuits.