Cysteamine pre-treatment reduces pentylenetetrazol-induced plasticity and epileptiform discharge in the CA1 region of rat hippocampal slices

Brain Res. 2002 Nov 15;955(1-2):98-103. doi: 10.1016/s0006-8993(02)03371-1.

Abstract

The effects of prior treatment of cysteamine, a somatostatin inhibitor, on pentylenetetrazol (PTZ) induced epileptic and plastic changes in CA1 excitability were examined. Population spikes were evoked by activation of Schaffer collaterals with a range of stimulation intensities. Changes in the population spike and epileptiform amplitudes were used as indices to quantify the effects of PTZ exposure in the control and cysteamine pre-treated slices. Cysteamine pre-treatment decreased baseline CA1 population spike amplitude following high intensity stimulation of Schaffer collaterals. Following PTZ application directly to the slices, cysteamine diminished the increased population spike and epileptiform amplitudes which were normally observed following collateral stimulation. Magnesium-free medium induced epileptiform activity was also significantly reduced with cysteamine pre-treatment. It is concluded that somatostatin may be involved in PTZ-induced epileptic and plastic changes in CA1 excitability.

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Animals
  • Cysteamine / pharmacology*
  • Cysteamine / therapeutic use
  • Epilepsy / chemically induced*
  • Epilepsy / drug therapy
  • Epilepsy / physiopathology
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • Hippocampus / drug effects*
  • Hippocampus / physiology
  • In Vitro Techniques
  • Male
  • Neuronal Plasticity / drug effects*
  • Neuronal Plasticity / physiology
  • Pentylenetetrazole / adverse effects*
  • Rats

Substances

  • Cysteamine
  • Pentylenetetrazole