Differential effects of enflurane on Glu- and ACH-induced chloride currents in Aplysia neurons.
The primary site of anesthetic action remains controversial. In addition to non-specific actions of hydrophobic substances on the membrane, specific effects of volatile anesthetics on neuronal activity have been reported. In the present study, effects of enflurane on the chloride currents (ICl) induced by L-glutamic acid (Glu) and acetylcholine (ACh) in isolated Aplysia neurons were examined, using the 'concentration clamp' technique. Enflurane increased the peak amplitude of the ICl induced by low concentrations of Glu but decreased those evoked by higher concentrations of the agonist. The anesthetic accelerated both activation and desensitization phases of the Glu-induced ICl. On the other hand, the ACh-induced ICl in the same neuron was depressed in an uncompetitive manner in the presence of enflurane. The desensitization phase was not affected, although the activation phase became more rapid and the mean open time obtained by noise analysis was shortened. These results suggest the existence of specific steps in the process of activation and desensitization of channels, at which the volatile anesthetic exerts differential effects on the postsynaptic currents.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D001048:Aplysia; D002712:Chlorides / Q000502:physiology*; D004737:Enflurane / Q000494:pharmacology*; D005724:Ganglia / Q000166:cytology / Q000502:physiology; D005971:Glutamates / Q000502:physiology*; D018698:Glutamic Acid; D008564:Membrane Potentials; D009474:Neurons / Q000502:physiology*
D002712:Chlorides; D005971:Glutamates; D018698:Glutamic Acid; D004737:Enflurane; D000109:Acetylcholine