GABAergic disinhibition facilitates polysynaptic excitatory transmission in rat anterior cingulate cortex

Biochem Biophys Res Commun. 2005 Dec 23;338(3):1634-9. doi: 10.1016/j.bbrc.2005.10.132. Epub 2005 Nov 2.

Abstract

Various studies implicate the anterior cingulate cortex (ACC) in processing pain. Combining whole-cell patch clamp recordings in rat ACC slices and a formalin-induced conditioned place avoidance (F-CPA) behavioral model, the present study was to address the effect of GABA(A) receptors on excitatory transmission to ACC layer V neurons and its possible functional significance related to pain. Removal of GABA(A) inhibition by bicuculline (10 microM) induced a novel long-lasting response in layer V neurons, which could be blocked by high divalent extracellular solution and was sensitive to relatively higher rate stimuli. Co-application of NMDA receptor antagonist APV (50 microM) and non-NMDA receptor antagonist DNQX (10 microM) completely blocked the responses. Enhancement of inhibition by intra-ACC microinjection of muscimol abolished the acquisition of F-CPA without affecting formalin-induced acute nociceptive responses. These results suggest that GABA(A) inhibition may be involved in pain-related aversion by modulating glutamate-mediated excitatory transmission in the ACC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bicuculline / pharmacology
  • Cerebral Cortex / metabolism*
  • Electrophysiology
  • Patch-Clamp Techniques
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Glutamate / metabolism
  • Synaptic Transmission* / drug effects
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • Receptors, Glutamate
  • gamma-Aminobutyric Acid
  • Bicuculline