Spontaneous sharp waves in human neocortical slices excised from epileptic patients

Brain. 1998 Jun:121 ( Pt 6):1073-87. doi: 10.1093/brain/121.6.1073.

Abstract

Human neocortical temporal lobe tissue resected for treatment of pharmacoresistant epilepsy was investigated. In slices prepared from this tissue, field potentials sometimes superimposed by population spikes were found to appear spontaneously. In individual slices, they were generalized or highly localized to a field of approximately 200 microns in diameter. Synchronous with these potentials, hyperpolarizing and depolarizing postsynaptic potentials were recorded from neurons in the vicinity of the field potential electrode. Hyperpolarizing postsynaptic potentials appeared to be mainly chloride mediated. All potentials, i.e. sharp field potentials as well as postsynaptic potentials, were reversibly suppressed by blockade of the non-NMDA (non-N-methyl-D-aspartate) glutamate-subreceptor and of the GABAA (gamma-aminobutyric acid) receptor, and by application of the organic calcium channel blocker verapamil. By contrast, all potentials remained unaffected by blockade of the NMDA glutamate-subreceptor and the GABAB receptor. The antiepileptic drugs carbamazepine and phenytoin failed to suppress the spontaneous potentials at therapeutic concentrations. Washout of Mg2+ from the superfusate left the spontaneous potentials unchanged or converted them to ictal-type discharges. This epileptiform activity was not suppressed, but augmented by blockade of the GABAA receptor. As a whole, the spontaneously appearing field potentials may be assumed to reflect a state of increased neuronal synchronization.

MeSH terms

  • Action Potentials / physiology
  • Adolescent
  • Adult
  • Anticonvulsants / pharmacology
  • Calcium Channels / physiology
  • Child
  • Electric Stimulation
  • Electrophysiology
  • Epilepsy / physiopathology*
  • Female
  • Humans
  • In Vitro Techniques
  • Male
  • Middle Aged
  • Receptors, GABA / physiology
  • Receptors, Glutamate / physiology
  • Synaptic Transmission / physiology
  • Temporal Lobe / drug effects
  • Temporal Lobe / physiopathology*

Substances

  • Anticonvulsants
  • Calcium Channels
  • Receptors, GABA
  • Receptors, Glutamate