Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

Eur J Neurosci. 2007 Dec;26(12):3571-82. doi: 10.1111/j.1460-9568.2007.05962.x. Epub 2007 Dec 4.


The hippocampus plays a primary role in temporal lobe epilepsy, a common form of partial epilepsy in adults. Recent studies, however, indicate that extrahippocampal areas such as the perirhinal and insular cortices represent important participants in this epileptic disorder. By employing field potential recordings in the in vitro 4-aminopyridine model of temporal lobe epilepsy, we have investigated here the contribution of glutamatergic and GABAergic signaling to epileptiform activity in these structures. First, we provide evidence of epileptiform synchronicity between the perirhinal and insular cortices, and resolve some pharmacological and network mechanisms involved in sustaining the interictal- and ictal-like discharges recorded there. Second, we report that in the absence of ionotropic glutamatergic transmission, GABAergic networks produce synchronous potentials that spread between the perirhinal and insular cortices. Finally, we have established that such activity is modulated by activating micro-opioid receptors. Our findings support clinical and experimental evidence concerning the involvement of the perirhinal and insular cortex networks in temporal lobe epilepsy, and provide observations that may impact research focussing on the role of the insular cortex in nociception.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 4-Aminopyridine
  • Action Potentials
  • Animals
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / physiopathology*
  • Cortical Synchronization*
  • Epilepsy, Temporal Lobe / chemically induced
  • Epilepsy, Temporal Lobe / metabolism
  • Epilepsy, Temporal Lobe / physiopathology*
  • Glutamic Acid / metabolism
  • Hippocampus / physiopathology
  • In Vitro Techniques
  • Male
  • Nerve Net / metabolism
  • Nerve Net / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, GABA-A / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Receptors, Opioid, mu / metabolism
  • Signal Transduction
  • gamma-Aminobutyric Acid / metabolism


  • Receptors, GABA-A
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Opioid, mu
  • Glutamic Acid
  • gamma-Aminobutyric Acid
  • 4-Aminopyridine