1. Intra-axonal recording and electron microscopy were applied to intramuscular myelinated axons in lizards and rats to investigate factors that influence the amplitude and time course of the depolarizing after-potential. 2. Depolarizing after-potentials in lizard axons had larger peak amplitudes and longer halfdecay times than those recorded in rat axons (mean values 10 mV, 35 ms in lizard; 3 mV, 11 ms in rat). These differences were not due to differences in temperature, resting potential or action potential amplitude or duration. 3. For a given axon diameter, the myelin sheath in lizard fibres was thinner and had fewer wraps than in rat fibres. There was no significant difference in myelin periodicity. Calculations suggest that the thinner myelin sheath accounts for < 30% of the difference between depolarizing after-potential amplitudes recorded in lizard and rat axons. 4. Consistent with a passive charging model for the depolarizing after-potential, the half-time of the passive voltage transient following intra-axonal injection of current was shorter in rat than in lizard axons. 5. Aminopyridines prolonged the falling phase of the action potential and increased the amplitude of the depolarizing after-potential in both types of axon. 6. During repetitive stimulation the depolarizing after-potentials following successive action potentials exhibited little or no summation. Axonal input conductance in the interspike interval increased during the train. 7. These findings suggest that the amplitude and time course of the depolarizing afterpotential are influenced not only by the passive properties of the axon and myelin sheath, but also by persisting activation of axolemmal K+ channels following action potentials.

SUMMARY1. Intra-axonal recordings were obtained from myelinated axons innervating a lizard skeletal muscle.2. Bath application of tetraethylammonium (TEA, 1-10 mM) depolarized the resting potential, prolonged the action potential and increased the amplitude and duration of the ensuing passive depolarizing after-potential (DAP) in a dosedependent and reversible manner. TEA increased the axonal input resistance and the slow time constant of the passive voltage response, not only in depolarized axons, but also in resting and hyperpolarized axons. The resting input resistance was tripled in 10 mM-TEA.3. TEA's effects on the resting potential and action potential usually approached a steady state within 5 min, whereas TEA's effects on input resistance and on the amplitude and time course of the DAP increased progressively for 10-15 min or more, and persisted for 10-15 min after removal of TEA from the bath.4. 4-Aminopyridine (4-AP, 1 mM), which prolonged the action potential by about the same extent as 10 mM-TEA, did not depolarize the resting potential or increase the resting input resistance, and produced a much smaller increase in DAP time course than 10 mM-TEA. Gallamine (1 mM) had effects more similar to those of TEA.5. These results suggest that the resting input conductance and DAP time course in lizard motor axons are controlled in part by K+ channels that are blocked by TEA and gallamine, but not by 4-AP. The slow development of the TEA-induced increase in input resistance and DAP time course suggests that some of these channels are located in paranodal or internodal axolemma.6. In TEA and gallamine additional depolarizing potentials were superimposed on the falling phase of the action potential and on the passive DAP. These superimposed potentials were abolished by 1 mM-Mn2+, and were probably caused by Ca2+ influx into motor terminals.

The effects of furosemide on action potentials and responses to several neurotransmitters have been studied in the neurons of Aplysia. Furosemide (10(-7) and 10(-3) M) does not visibly affect the normal action potential in R15 neurons. However, when TTX (30 microM) is used to block the sodium component in R15, the remaining spike (presumably the calcium component) is increased in amplitude in the presence of furosemide. Furosemide also alters transmitter-induced conductances. Furosemide greatly reduces the amplitude and shifts, in a depolarizing direction, the reversal potential of chloride-dependent responses to gamma-aminobutyric acid (GABA) and acetylcholine (ACh). This suggests that furosemide both blocks the chloride channel and inhibits a chloride pump. ACh-induced sodium responses were also reduced by furosemide but to a lesser extent than chloride responses. The potassium response to ACh and a voltage-dependent calcium response to serotonin were not altered. These results indicate that furosemide could alter synaptic responses both presynaptically by enhancement of calcium flux during the action potential and postsynaptically by blockade of chloride and sodium conductances.

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