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pubmed:abstractText |
A delayed depolarization following the impulse can be recorded intracellularly from mature Rohon-Beard neurones in the spinal cord of Xenopus tadpoles, in response both to brief intracellularly injected current pulses and to antidromic stimulation. Evidence is presented suggesting that this delayed depolarization is unlikely to be due to the action of a chemical synapse, activation of a voltage-dependent conductance in the cell body, increased extracellular potassium, or electrotonic coupling. Hyperpolarization of the cell body during antidromic stimulation eliminates the action potential normally generated there, and reveals an impulse arising at some distance along a neurite. When an action potential is produced in the cell body, its repolarizing phase sculpts a delayed depolarization from this impulse in the neurite. The depolarization is enhanced by pressure applied to the neurites near the cell body, presumably by reducing the distal spread of current, and yields multiple action potentials. Although long current pulses usually produce only a single spike, small quantities of La3+ enhance the size of the depolarization and cause repetitive firing. The relation of impulse frequency to injected current shows a non-linearity consistent with the summation of the delayed depolarization and the depolarization by the injected current. The non-linearity is eliminated upon removal of delayed depolarization by hyperpolarizing current pulses injected after each impulse. The enhancement of the depolarization by La3+ is not the only cause of repetitive firing; La3+ also produces an effective reduction in conductance for outward currents. This depolarization may play a role in the normal firing behaviour of Rohon-Beard neurones; when repetitive firing results naturally in response to long current pulses the delayed depolarization is observed to be large.
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