Aliphatic alcohols increase the decay rate of glutamate-activated currents at the crayfish neuromuscular junction.
Excitatory junction currents produced by glutamate were recorded with an extracellular electrode at the excitatory neuromuscular junction of the crayfish. The currents decayed more quickly as the membrane was hyperpolarized. The direction of the voltage sensitivity of the decay phase is thus opposite to that found for acetylcholine-activated currents at the amphibian endplate. The aliphatic alcohols ethanol to octanol all increased the rate of decay of the currents. The effects of the short chain alcohols were opposite to their actions at the toad endplate, where ethanol to pentanol prolong the currents. This observation was explained in terms of the opposite direction of the voltage sensitivity in the two preparations. For each alcohol, the relationship between the half-decay time of the currents (t 1/2) and alcohol concentration was exponential. The potency of each alcohol in decreasing t 1/2 was exponentially related to carbon chain length, which would be predicted if the effects of the alcohols were directly related to their concentration in the lipid phase of the membrane. These findings are consistent with the ideas that the alcohols may alter membrane polarizability or change membrane fluidity in the vicinity of the channels.
D000438:Alcohols / Q000494:pharmacology*; D000818:Animals; D003400:Astacoidea / Q000502:physiology*; D003208:Concanavalin A / Q000494:pharmacology; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D013329:Structure-Activity Relationship
D000438:Alcohols; D005971:Glutamates; D003208:Concanavalin A; D018698:Glutamic Acid