Epileptiform activity in hippocampal slice cultures with normal inhibitory synaptic drive

Alfred T. Malouf, Carol A. Robbins, Philip A Schwartzkroin

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

The synaptic events responsible for epileptiform burst discharge are often difficult to define. Blockade of inhibition has been used to produce epileptiform events, but it is unclear whether increased excitatory activity in the presence of normal inhibition can also result in burst discharge. In the hippocampal slice culture preparation, a small percentage of cultures exhibit spontaneous bursts. To determine whether the absence of inhibitory postsynaptic potentials (IPSPs) is responsible for these spontaneous bursts, we applied the glutamate antagonist, kynurenic acid (KYN) to block burst activity, and unmask any underlying IPSPs. KYN (10 mM) quickly reduced synaptic activity with concomitant loss of burst discharge. Washout of KYN resulted in a gradual return of synaptic activity, during which time both fast and slow IPSPs were clearly observed. As burst activity returned to control levels, excitatory postsynaptic potentials (EPSPs) were increasingly superimposed within the inhibitory events, obscuring (but not eliminating) the IPSPs. In these hippocampal slice cultures, therefore, epileptiform bursts appear to be the result of an abnormally high level of excitatory synaptic drive, not a reduction in inhibition.

Original languageEnglish (US)
Pages (from-to)76-80
Number of pages5
JournalNeuroscience Letters
Volume108
Issue number1-2
DOIs
StatePublished - Jan 1 1990
Externally publishedYes

Keywords

  • CA3 pyramidal neuron
  • Epileptiform activity
  • Hippocampus
  • Inhibitory postsynaptic potential
  • Kynurenic acid
  • Paroxysmal depolarization shift
  • Slice culture

ASJC Scopus subject areas

  • Neuroscience(all)

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