Actions of Ethanol on Voltage-Sensitive Sodium Channels: Effects on Neurotoxin-Stimulated Sodium Uptake in Synaptosomes
Abstract
Exposure of rat brain synaptosomes to ethanol in vitro reduced the neurotoxin-stimulated uptake of 22Na(+). This effect of ethanol was concentration-dependent, occurred with concentrations of ethanol achieved in vivo and was fully reversible. The inhibitory effect of ethanol on neurotoxin- stimulated sodium uptake was due to a decrease in the maximal effect of the neurotoxins. Ethanol reduced the rate of batrachotoxin-stimulated sodium uptake when measured at 3, 5 and 7 but not 10 or 20 sec after the addition 22Na(+). In a series of aliphatic alcohols, there was a good correlation between potency for inhibition of batrachotoxin-stimulated 22Na(+) uptake and the membrane/buffer partition coefficient, suggesting that a hydrophobic site in the membrane was involved in the action of the alcohols. Ethanol did not affect the scorpin venom-induced enhancement of batrachotoxin-stimulated sodium uptake. The inhibitory potency of tetrodotoxin was also unaffected by ethanol. These results demonstrate that ethanol has an inhibitory effect on neurotoxin-stimulated sodium influx occurring in voltage-sensitive sodium channels of brain tissue.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 1985
- Accession Number
- ADA153883
Entities
People
- Michael J. Mullin
- Walter A. Hunt
Organizations
- Armed Forces Radiobiology Research Institute