Item

ITEM ACTIONS

This item is discarded!DetailsSummary

Discarded

Journal Article

Effects of NMDA antagonists on picrotoxin−low Mg2+− and low Ca2+−induced epileptogenesis and on evoked changes in extracellular Na und Ca concentrations in rat hippocampal slices

MPS-Authors

/persons/resource/persons93955

Köhr, Georg
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Directly responsible to the Managing Director, Max Planck Institute for Medical Research, Max Planck Society;
Georg Köhr Group, Max Planck Institute for Medical Research, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Köhr, G., & Heinemann, U. (1989). Effects of NMDA antagonists on picrotoxin−low Mg2+− and low Ca2+−induced epileptogenesis and on evoked changes in extracellular Na und Ca concentrations in rat hippocampal slices. Epilepsy Res., 4(3), 187-200. doi:10.1016/0920-1211(89)90003-X.

Abstract

The anticonvulsant properties of ketamine and 2−APV were compared on 3 types of convulsant activity in hippocampal area CA1: the picrotoxin−epilepsy, the low magnesium epilepsy and the low calcium epilepsy. In particular the spontaneous activity, the synaptically evoked responses and the changes in [Ca2+]0 were examined, since in many cases of epilepsy, Ca2+ uptake into cells is enhanced. In normal medium, ketamine and 2−APV have nearly no effect on stimulus evoked decreases in [Ca2+]0, although they clearly depress NMDA−induced ionic changes. However, ketamine and 2−APV prevent to some extent the augmentation of stimulus−induced changes in [Ca2+]0, observed after treating slices with picrotoxin or Mg2+−free medium. This extra Ca2+ uptake is probably mediated by NMDA operated channels. Our findings also show that ketamine, like 2−APV, has a stronger anticonvulsant effect on the low Mg−than on the picrotoxin−induced epileptiform activity. Responses to iontophoretically applied NMDA are facilitated in the ‘low calcium epilepsy' and can be selectively blocked by ketamine. Spontaneous epileptiform activity occurring in low calcium can be blocked by ketamine only when some synaptic transmission is still present