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Kindled seizure-evoked somatostatin release in the hippocampus: inhibition by MK-801.

Authors
  • Marti, M
  • Bregola, G
  • Binaschi, A
  • Gemignani, A
  • Simonato, M
Type
Published Article
Journal
Neuroreport
Publisher
Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins
Publication Date
Sep 28, 2000
Volume
11
Issue
14
Pages
3209–3212
Identifiers
PMID: 11043550
Source
Medline
License
Unknown

Abstract

The aim of this study was to evaluate the contribution of ionotropic glutamate receptors to kindled seizure-evoked somatostatin release in the hippocampus, using a microdialysis approach. Basal and amygdala stimulation-evoked somatostatin-like immunoreactivity (-LI) release was significantly greater in kindled compared to naive rats. In naive rats, neither hippocampal perfusion with the selective AMPA/kainate receptor antagonist GYKI 52466 nor with the selective NMDA receptor antagonist MK-801 affected behavior, EEG, or somatostatin-LI release. In kindled rats, GYKI 52466 was still devoid of any effect, while MK-801 significantly decreased stimulus-evoked (but not basal) somatostatin-LI efflux. MK-801 produced identical effects when injected i.p. This study provides the first direct evidence that kindled seizure-evoked somatostatin release in the hippocampus is partly NMDA receptor dependent.

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