Ionic mechanisms underlying the firing properties of rat neonatal motoneurons studied in vitro.
Ionic mechanisms underlying the firing properties of spinal motoneurons of neonatal rats (postnatal days 3-10) have been investigated using a hemisected, in vitro spinal cord preparation. These results demonstrate the presence of a high-threshold voltage-dependent calcium response and partial sodium-dependent spikes. The calcium current is evident during the falling phase of the action potential and is the major component of the after-depolarizing potential. The subsequent increase in intracellular calcium concentration activates a calcium-dependent potassium conductance (gK-Ca), the major component of the after-hyperpolarizing potential. The gCa, by activating gK-Ca, is the primary determinant of firing rate in neonatal motoneurons. For, when gCa was blocked by Cd2+, the interspike interval decreased, the maximum firing rate and the slope of the firing frequency-injected current relation increased. The calcium current is particularly robust during the first few postnatal days; during this period, tetrodotoxin resistant action potentials can be elicited by direct stimulation under control conditions. In animals older than 5 days such calcium spikes could be elicited only after decreasing gK with intracellular Cs+ or extracellular tetraethylammonium. This was the case even when 1 mM of the bath CaCl2 was replaced with BaCl2. The rising phases of calcium spikes recorded from neurons in both age groups demonstrate several components suggesting the calcium spikes comprise several discrete events, which probably originate across the dendritic membrane. When gK was decreased by bath application of tetraethylammonium+ and Cs+, neonatal motoneurons generated prolonged Ca-dependent spikes lasting for up to 6 s. Repolarization of Ca spikes occurred in two stages, the first was rapid (-2.11 +/- 0.8 V/s, n = 6) but incomplete. The second, was slower (-0.01 +/- 0.003 V/s, n = 5) and returned the membrane potential to the resting level after about 1-2 s. It is suggested that accumulation of extracellular potassium may contribute to the slow phase of repolarization. Motoneurons from the younger age group (3-5 days old) demonstrate all-or-none partial spikes rising from the after-depolarization of directly elicited sodium-dependent action potentials. Similar partial spikes were elicited from neurons from older animals during intracellular Cs+ loading. The partial spikes had faster rates of rise than the tetrodotoxin-resistant spikes and were not seen after tetrodotoxin treatment, suggesting that they are sodium-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D001464:Barium / Q000378:metabolism; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology / Q000502:physiology; D002412:Cations / Q000494:pharmacology / Q000502:physiology*; D002586:Cesium / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology; D009046:Motor Neurons / Q000187:drug effects / Q000254:growth & development / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000494:pharmacology / Q000502:physiology; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D002412:Cations; D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D002104:Cadmium; D002586:Cesium; D001464:Barium; D013779:Tetrodotoxin; D012964:Sodium; D002118:Calcium