Removal of rapid sensory adaptation from an insect mechanoreceptor neuron by oxidizing agents which affect sodium channel inactivation

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Abstract
The femoral tactile spine of the cockroach is a mechanoreceptor with a single sensory neuron. The response to a step movement is a burst of action potentials which decays to zero in about 1 s. This rapid adaptation is a property of the action potential initiating region of the neuron. The oxidizing agents chloramine-T andN-chlorosuccinimide selectively and irreversibly remove sodium channel inactivation from neurons in several preparations and are believed to act by oxidation of methionine or cysteine residues in the proteins of the sodium channel. Chloramine-T andN-chlorosuccinimide, applied for a controlled time period, eliminated the rapid adaptation of the tactile spine neuron to an electrical depolarization. After treatment it fired tonically in response to a steady current stimulus. Longer applications of the agents eventually raised the threshold for action potential initiation. Threshold behavior in the tactile spine neuron was characterized by measuring strength-duration relationships for stimulation with extracellular current pulses at the action potential initiating region. The two oxidizing agents caused a voltage-dependent modification of the dynamic threshold properties which led to the change from rapidly adapting to tonic behavior. Two stronger oxidizing agents,N-bromoacetamide andN-bromosuccinimide, raised the threshold of the neuron without removing rapid adaptation. These two agents act similarly to chloramine-T andN-chlorosuccinimide on sodium inactivation in other neurons but are believed to oxidize the tryptophan, tyrosine and histidine residues of proteins in addition to cysteine and methionine. These results suggest that a form of sodium channel inactivation is responsible for rapid sensory adaptation in this neuron, but one which is different in time course and chemical sensitivity to the sodium inactivation seen in many other neurons.