English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Effects of the tetronic acid derivatives AO33 (losigamone) and AO78 on epileptiform activity and on stimulus-induced calcium concentration changes 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;

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. (1990). Effects of the tetronic acid derivatives AO33 (losigamone) and AO78 on epileptiform activity and on stimulus-induced calcium concentration changes in rat hippocampal slices. Epilepsy Research, 7(1), 49-58. doi:10.1016/0920-1211(90)90053-X.


Cite as: https://hdl.handle.net/21.11116/0000-0000-7379-7
Abstract
The effects of members of a new class of anticonvulsants, the tetronic acid derivatives, were studied in 3 in vitro models of epileptogenesis in rat hippocampal slices; the picrotoxin, the low magnesium and the low calcium model. The effects of AO33 (losigamone) and AO78 on stimulus-induced decreases in extracellular calcium concentration were also investigated. In all 3 models of epileptogenesis, both drugs blocked spontaneous and reduced stimulus-induced epileptiform discharges dose dependently and reversibly. Stimulus-induced changes in [Ca2+]0 were markedly diminished by these agents. The fact that the tetronic acid derivatives block the low Ca seizure-like events which develop independently from chemical synaptic transmission suggests that these agents have non-synaptic or direct membrane actions with subsequently reduced cellular excitability