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Memory for fear extinction requires mGluR5-mediated activation of infralimbic neurons

Darah E Fontanez-Nuin1, Edwin Santini, Gregory J Quirk

  • 1Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto Rico 00732-7004.

Cerebral Cortex (New York, N.Y. : 1991)
|August 14, 2010
PubMed

Insights

Metabotropic glutamate receptor type 5 (mGluR5) activation in the infralimbic cortex enhances fear extinction memory recall. Targeting mGluR5 may offer new treatments for anxiety disorders.

Area of Science:

  • Neuroscience
  • Behavioral Neuroscience
  • Pharmacology

Background:

  • Fear extinction memory consolidation involves N-methyl D-aspartate (NMDA) receptor-dependent bursting in the medial prefrontal cortex (mPFC).
  • Metabotropic glutamate receptor type 5 (mGluR5) antagonists reduce mPFC bursting, while agonists enhance NMDA receptor currents, suggesting a role for mGluR5 in fear extinction.

Purpose of the Study:

  • To investigate the role of mGluR5 stimulation in the infralimbic (IL) region of the mPFC in fear extinction recall.
  • To determine if mGluR5 activation directly enhances burst firing in IL neurons.

Main Methods:

  • Rats received systemic or intra-IL injections of an mGluR5 antagonist (MPEP) before extinction training.
  • Patch-clamp electrophysiology was used in prefrontal slices to examine the effects of an mGluR5 agonist (CHPG) on IL neuronal bursting.
  • Effects of CHPG on NMDA currents were also assessed.

Main Results:

  • Systemic or intra-IL MPEP administration impaired fear extinction recall the following day, despite normal within-session extinction.
  • The mGluR5 agonist CHPG increased intrinsic bursting in IL neurons, which correlated with a reduced slow afterhyperpolarization.
  • CHPG-induced bursting was blocked by MPEP and did not involve potentiation of NMDA receptor currents.

Conclusions:

  • mGluR5 stimulation enhances IL neuronal bursting independently of NMDA receptor potentiation, contributing to fear extinction recall.
  • The mGluR5 receptor represents a potential therapeutic target for enhancing extinction-based treatments for anxiety disorders.

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