In vitro and in vivo depolarization coupled efflux of ascorbic acid in rat brain preparations.
The depolarization-coupled efflux of endogenous ascorbate is demonstrated using rat synaptosome preparations and a rat cortical cup method. Ascorbate and catecholamines (monitored as a methodological control) were quantitated by high pressure liquid chromatography with electrochemical detection. In vitro potassium ion induces ascorbate efflux in a concentration-dependent, although calcium ion-dependent, manner. Veratridine also induces ascorbate efflux and its effect can be blocked by tetrodotoxin. In vivo, ascorbate efflux was likewise stimulated by increased potassium ion and by veratridine. In addition, electrical stimulation of medial lemniscus was accompanied by an increased efflux of ascorbate from somatosensory cortex. These results are intriguing in light of the recent evidence for the interaction of ascorbate with several neurotransmitter systems.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D002525:Cerebellar Cortex / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D004558:Electric Stimulation; D005260:Female; D008297:Male; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission / Q000187:drug effects; D013574:Synaptosomes / Q000378:metabolism; D014701:Veratridine / Q000494:pharmacology
D014701:Veratridine; D001205:Ascorbic Acid; D011188:Potassium