Evoked depolarizing and hyperpolarizing potentials in reticulospinal axons of lamprey.

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Abstract
1. Intracellular recordings were made from reticulospinal axons (Müller axons) in the lamprey spinal cord. Electrical stimuli applied to the spinal cord surface elicited depolarizing and hyperpolarizing 'synaptic‐like' potentials in Müller axons. The physiological basis of these evoked potentials was investigated. 2. The depolarizing response was not the result of increased extracellular K, as demonstrated by the constancy of the undershoot of the axonal action potential during the depolarization, by the failure of the response to summate during repetitive stimulation and by the failure of the response amplitude to vary as predicted when the [K] of the saline was varied. 3. When the membrane potential of the axon was varied by passing current through a micro‐electrode, the amplitude of the depolarizing evoked potential decreased at membrane potentials positive to the resting potential and increased up to a maximum when the axon was hyperpolarized by about 10 mV. The extrapolated 'reversal potential' for the depolarizing response was about 15 mV positive to the normal ‐80 mV resting potential of the axon. However, the amplitude of the response did not continue to grow with hyperpolarizations greater than 10 mV, and, thus, the response did not behave as would a normal depolarizing synaptic potential. 4. Müller axons make numerous electrical synapses with spinal motoneurones and interneurones, and this suggested that the depolarizing response might be a coupling potential. In agreement with this idea, quantitative correspondence was found between changes in the input resistance of the axon produced by the depolarizing response and the variation in the depolarizing response amplitude. Thus, although the depolarizing response mimicked in some ways the behaviour of an excitatory synaptic potential, we conclude that it is a coupling potential. 5. The hyperpolarizing response also appeared to be a coupling potential. Its amplitude was not changed by hyperpolarizing the axon up to 30 mV and was decreased by depolarizing the axon sufficiently to decrease the axon's input resistance. 6. It is proposed that both depolarizing and hyperpolarizing evoked potentials in lamprey Müller axons are a result of passive flow of current from cells activated by the spinal cord stimulus and electrically coupled to Müller axons.