NIFEDIPINE-CONOTOXIN-SENSITIVE AND OMEGA-CONOTOXIN-SENSITIVE CA2-PIG SUBSTANTIA NIGRA-PARS-COMPACTA NEURONS( CONDUCTANCES IN GUINEA)

1. The membrane properties of substantia nigra pars compacta (SNc) neu rones were recorded in guinea-pig in vitro brain slices. 2. In the pre sence of tetrodotoxin (TTX) a Ca2+-dependent slow oscillatory potentia l (SOP) was generated. Application of 0.5-20 mum nifedipine abolished both spontaneous and evoked SOPs. A tetraethylammonium chloride (TEA)- promoted high-threshold Ca2+ spike (HTS) was little affected by nifedi pine. On the other hand, omega-conotoxin applied either locally or via the perfusion medium (1-10 mum) blocked a part of the HTS, but it did not alter the SOP. 3. In normal medium nifedipine blocked the spontan eous discharge, decreased the interspike interval (ISI) recorded durin g depolarizing current injections and selectively reduced the slow com ponent of the spike after-hyperpolarization (AHP). omega-Conotoxin dec reased both the rising and falling slopes of the normal action potenti al, reduced the peak amplitude of the spike AHP, and, in some of the n eurones, reduced the ISI during depolarization. The Na+ spikes recorde d in Ca2+-free medium were not altered by omega-conotoxin. 4. The SOP was not blocked by octanol (100-200 mum), amiloride (100-250 mum), or Ni2+ (100-300 mum). However, at 500 mum Ni2+ attenuated the SOP. 5. Ap plication of apamin (0-5-2.0 mum) induced irregular firing or bursting . abolished the slow component of the spike AHP and reduced its peak a mplitude. In the presence of TTX and apamin long-duration plateau pote ntials occurred, which were subsequently blocked by nifedipine. 6. In Ca2+-free, Co2+-containing medium TTX-sensitive spikes and voltage pla teaux were generated by depolarizing current pulses. It is suggested t hat a persistent Na+ conductance underlies the plateaux, which may be co-activated during the SOP. 7. The results suggest that the Ca2+ curr ents underlying the SOP and the HTS are different and that they activa te at least two Ca2+-dependent K+ conductances. These conductances pla y major roles in the maintenance of spontaneous discharge and in contr ol of membrane excitability.