Barium ions induce prolonged plateau depolarizations in neurosecretory neurones of the adult rat supraoptic nucleus.
The occurrence and ionic basis of prolonged plateau depolarizations were studied during intracellular recordings obtained from thirty-nine supraoptic nucleus (s.o.n.) neurosecretory neurones in perfused explants of rat hypothalamus. Replacement of Ca2+ by Ba2+ in the perfusion media enhanced the shoulder on the repolarization phase of the action potentials in all of eleven cells tested. In Ba2+, spike durations increased as the holding membrane potential was made more positive, resulting in plateaux lasting up to 100 s. These plateaux were characterized by a sustained but slowly decaying absolute potential near 0 mV from which there appeared frequent spontaneous hyperpolarizing transients. A membrane resistance decrease of more than 50% was observed at the onset of a plateau, with gradual restoration during the plateau. Injection of Cs+ into twenty-one cells abolished the spike frequency adaptation and after-hyperpolarization associated with current-evoked bursts of action potentials. Mean spike duration after Cs+ injection increased from 2.5 +/- 0.3 ms to 68 +/- 9 ms (S.E. of mean). Addition of 4-5 mM-tetraethylammonium (TEA) to the perfusion media further increased the spike duration of nine Cs+-injected cells to 320 +/- 70 ms. No further increase could be obtained by doubling the concentration of TEA and/or by the addition of 0.2-0.5 mM-4-aminopyridine to the media. Although spike duration was greatly prolonged during such extensive blockade of K+ channels, plateau potentials lasting for longer than 1 s were observed only when Ba2+ was eventually added to the perfusion media. The special property of Ba2+ that leads to the formation of plateau potentials in s.o.n. neurones is therefore not restricted to its ability to reduce K+ conductances but may reside in its reduced effectiveness as a mediator of Ca2+-dependent inactivation of Ca2+ channels. Injection of Cs+ into s.o.n. neurones increased the slope of their current-voltage relationship below -60 mV from 148 +/- 15 to 257 +/- 41 M omega (S.E. of mean) and eliminated the outward rectification present at potentials above -60 mV. K+ currents are presumably active near the resting potential of these cells. Addition of Ba2+ to the perfusion media revealed a Cd2+-sensitive inward rectification above but not below ca. -55 mV. A slowly inactivating Ba2+ current is therefore carried through Ca2+ channels at potentials above -55 mV.(ABSTRACT TRUNCATED AT 400 WORDS)
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001464:Barium / Q000494:pharmacology*; D002104:Cadmium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013495:Supraoptic Nucleus / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D002104:Cadmium; D002586:Cesium; D001464:Barium; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D011188:Potassium