Excitatory junctional responses and glutamate responses at the crayfish neuromuscular junction in the presence of chlorisondamine.
At the crayfish neuromuscular junction chlorisondamine reduced the amplitude of both the excitatory junctional potential and the glutamate current in a dose-dependent manner in concentrations above 3 microM, and it is suggested that the drug is a powerful non-competitive antagonist for glutamate. Chlorisondamine did not act presynaptically on the crayfish neuromuscular junction. A double exponential decay of excitatory synaptic currents was observed in the presence of chlorisondamine, suggesting that this drug is an open channel blocker for the excitatory neurotransmitter. The glutamate current tail was prolonged in the presence of chlorisondamine. This prolongation increased with increasing iontophoretic current of glutamate. The rate of recovery from the refractory form of the glutamate receptor to the free reactive one was hardly affected by chlorisondamine. The inhibitory action of chlorisondamine on glutamate responses was voltage-dependent and hyperpolarization reduced the drug action. Chlorisondamine depressed the glutamate current even in Na-free, Ca-rich solution.
D000818:Animals; D003400:Astacoidea / Q000502:physiology; D002714:Chlorisondamine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000502:physiology*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D007473:Ion Channels; D018698:Glutamic Acid; D002714:Chlorisondamine