Potassium-depolarizatian-induced cytoplasmic [Ca2+] transients in freshly dissociated pyramidal neurones of the rat dorsal cochlear nucleus

The significance of voltage-activated Ca2+ currents in eliciting cytoplasmi c Ca2+ transients was studied in pyramidal neurones isolated from the rat d orsal cochlear nucleus using combined enzyme treatment/mechanical triturati on. Increases in cytoplasmic Ca2+ concentration ([Ca2+](i)) were evoked by K+-induced depolarizations (10-50 mM) and monitored by the Fura-2 fluorimet ric technique. The acutely dissociated neurones had a resting [Ca2+](i) of 17.2+/-0.5 nM. They possessed caffeine-sensitive Ca2+ stores which were emp ty at rest: these stores could be filled with Ca2+ entering from the extrac ellular space and were re-emptied quickly. The effects of various specific high-voltage-activated (HVA) Ca2+ channel antagonists (nifedipine, omega-ag atoxin IVA and omega-conotoxin GVIA) on [Ca2+](i) transients were tested. A nalysis of the blocking effects of these agents on the [Ca2+](i) transients indicates that, in the pyramidal neurones of the dorsal cochlear nucleus, N-type Ca2+ channels are primarily responsible for producing the depolariza tion-induced increases in [Ca2+](i).