Properties of a persistent inward current in normal and TEA-injected motoneurons.
1. Membrane currents of normal and TEA-injected cat lumbar motoneurons were investigated using the technique of somatic voltage clamp. 2. The current-voltage (I-V) relation of healthy motoneurons contains a region of negative slope conductance caused by a persistent inward current component (Ii). In the most striking examples, Ii is net inward at some potentials between 10 and 30 mV positive to resting potential. 3. Near its activation threshold (greater than or equal to 10 mV positive to rest), Ii does not decrement during prolonged voltage steps and, in most cells, activates very slowly. Ii amplitude increases and time to peak Ii decreases with further small increments of depolarization, and Ii decrements during sustained voltage steps. Maximum Ii amplitude occurs 20--30 mV positive to rest in most cells. Ii is not visible at sufficiently large depolarizations. 4. Ii appears to be mixed with potassium current components at nearly every potential where it is visible. These include a slow outward current first activated near Ii activation threshold, a fast outward current additonally activated at larger depolarizing potentials, and a fast, transient outward current that obscures the true onset of Ii at nearly every potential. 5. Ii is not carried by sodium entering via the fast, transient channels and is present after pharmacological blockage of sodium currents. It is proposed that Ii is predominantly carried by calcium ions. 6. The presence of inward tail currents after repolarization from potentials that activate a steady outward current suggest that Ii remains present but hidden at large depolarizations. Ii inactivation was further investigated in TEA-injected motoneurons since Ii and the tail currents are more prominent in these cells. 7. Conventional recordings from TEA-injected motoneurons suggest that a prolonged, postspike plateau potential is maintained by a persistent inward current. Voltage-clamp data can account for the principal features of the plateau potential. 8. Voltage-clamp results in TEA-injected motoneurons suggest that Ii is subject to little or no inactivation at potentials less than or equal to 30 mV positive to rest and to partial inactivation, at most, at higher potentials during steps lasting less than or equal to 100 ms. The apparent decay of Ii during sustained depolarization is caused by the development of a larger outward current. 9. Ii is similar in several ways to a persistent calcium current observed in some molluscan neurons. Theoretical and experimental results suggest that Ii is generated predominantly in a local region under voltage control and that the observed membrane currents govern somatic membrane potential and cell behavior.
D000818:Animals; D002415:Cats; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013116:Spinal Cord / Q000187:drug effects*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D012964:Sodium; D011188:Potassium