title: Block of glutamate-activated synaptic channels by curare and gallamine.
abstract: Excitatory junctional currents (e.j.cs) and glutamate-activated currents have been examined in voltage-clamped locust muscle fibres exposed to curare or gallamine. Although these drugs have little action on channel kinetics at the resting potential, there is an increasingly pronounced effect at hyperpolarized levels. In the presence of curare (5-100 microM), fibres held at hyperpolarized potentials showed e.j.cs with an initial 'fast component' followed by a 'slow tail'. In many fibres, hyperpolarization beyond -50 mV decreased the amplitude of the peak synaptic current; the decay time constant of the fast component was decreased by hyperpolarization while the time constant of the slow component was increased. Iontophoretic application of brief pulses of glutamate also produced two-component glutamate currents in these conditions. Gallamine was considerably more effective than curare, markedly altering the decay time and amplitude of the e.j.c. and the glutamate current at 1-5 microM. Its effects appeared qualitatively similar to those of curare. The observations are consistent with the idea that curare and gallamine produce a transient block of glutamate-activated synaptic channels.
mesh_terms: D000818:Animals; D003472:Curare / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists; D005703:Gallamine Triethiodide / Q000494:pharmacology*; D018698:Glutamic Acid; D006110:Grasshoppers; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects
chemical_list: D018691:Excitatory Amino Acid Antagonists; D007473:Ion Channels; D018698:Glutamic Acid; D003472:Curare; D005703:Gallamine Triethiodide