GABA-mediated synchronization in the human neocortex: Elevations in extracellular potassium and presynaptic mechanisms

J. Louvel, C. Papatheodoropoulos, A. Siniscalchi, I. Kurcewicz, R. Pumain, B. Devaux, B. Turak, V. Esposito, J. G. Villemeure, M. Avoli

Research output: Contribution to journalArticlepeer-review


Field potential and extracellular [K+] ([K+]o) recordings were made in the human neocortex in an in vitro slice preparation to study the synchronous activity that occurs in the presence of 4-aminopyridine (50 μM) and ionotropic excitatory amino acid receptor antagonists. Under these experimental conditions, negative or negative-positive field potentials accompanied by rises in [K+]o (up to 4.1 mM from a baseline of 3.25 mM) occurred spontaneously at intervals of 3-27 s. Both field potentials and [K+]o elevations were largest at approximately 1000 μm from the pia. Similar events were induced by neocortical electrical stimuli. Application of medium containing low [Ca2+]/high [Mg2+] (n = 3 slices), antagonism of the GABAA receptor (n = 7) or μ-opioid receptor activation (n = 4) abolished these events. Hence, they represented network, GABA-mediated potentials mainly reflecting the activation of type A receptors following GABA release from interneurons. The GABAB receptor agonist baclofen (10-100 μM, n = 11) reduced and abolished the GABA-mediated potentials (ID50 = 18 μM). Baclofen effects were antagonized by the GABAB receptor antagonist CGP 35348 (0.1-1 mM, n = 6; ID50 = 0.19 mM). CGP 38345 application to control medium increased the amplitude of the GABA-mediated potentials and the concomitant [K+]o rises without modifying their rate of occurrence. The GABA-mediated potentials were not influenced by the broad-spectrum metabotropic glutamate agonist (±)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (100 μM, n = 10), but decreased in rate with the group I receptor agonist (S)-3,5-dihydroxyphenylglycine (10-100 μM, n = 9). Our data indicate that human neocortical networks challenged with 4-aminopyridine generate glutamatergic-independent, GABA-mediated potentials that are modulated by μ-opioid and GABAB receptors presumably located on interneuron terminals. These events are associated with [K+]o elevations that may contribute to interneuron synchronization in the absence of ionotropic excitatory synaptic transmission.

Original languageEnglish
Pages (from-to)803-813
Number of pages11
Issue number4
Publication statusPublished - Aug 22 2001


  • [K]
  • GABA
  • Human cortex
  • Opioid receptors
  • Synchronization

ASJC Scopus subject areas

  • Neuroscience(all)


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