1. The involvement of sodium and calcium ions in the release of amino acid neurotransmitters from mouse cortical slices elicited by hyperforin.
- Author
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Marsh WL and Davies JA
- Subjects
- Animals, Aspartic Acid metabolism, Bridged Bicyclo Compounds, Calcium metabolism, Cerebral Cortex drug effects, Female, Glutamic Acid metabolism, Male, Mice, Mice, Inbred BALB C, Phloroglucinol analogs & derivatives, Potassium Channel Blockers, Potassium Channels drug effects, Potassium Channels metabolism, Sodium metabolism, Sodium Channel Blockers, Sodium Channels drug effects, Sodium Channels metabolism, Tetrodotoxin pharmacology, Veratridine pharmacology, gamma-Aminobutyric Acid metabolism, Antidepressive Agents pharmacology, Calcium physiology, Cerebral Cortex metabolism, Neurotransmitter Agents metabolism, Sodium physiology, Terpenes pharmacology
- Abstract
Hyperforin is currently considered to be the major active antidepressant constituent of the medicinal herb St. John's wort (Hypericum perforatum L.). The mechanism of action however, is still largely unknown, although the involvement of sodium and calcium has been recently inferred. In the present study hyperforin (5 microM) significantly potentiated the release of endogenous aspartate and glutamate from mouse cortical slices when stimulated by veratridine or potassium. Hyperforin (5 microM) also stimulated the release of aspartate, glutamate, serine, glycine and GABA when perfused on its own. Perfusion of the sodium channel blocker, tetrodotoxin (TTX) inhibited the effect of hyperforin, whereas removal of extracellular calcium potentiated the effect. Our observations suggests that hyperforin increases the overflow of neurotransmitters from mouse cerebral cortex possibly through facilitating the entry of sodium into the neurone which leads to the release of calcium from intracellular stores.
- Published
- 2002
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