Differential modulation of respiratory neuronal discharge patterns by GABA(A) receptor and apamin-sensitive K(+) channel antagonism.
Intracellular recordings were obtained from rat trigeminal motoneurons in slice preparations to investigate the role of calcium conductances in the depolarizing and hyperpolarizing spike afterpotential (ADP and mAHP, respectively). The mAHP was suppressed by bath application of 1 microM apamin, 2 mM Mn2+, and 2 mM Co2+, and also by intracellular injection of ethylene glycol-bis(b-aminoethylenether)-N,N,N',N'-tetraacetic acid (EGTA), suggesting that the potassium conductance generating the mAHP is activated by Ca2+ influx. Mn2+ (2 mM) or Cd2+ (500 microM) reduced the ADP, whereas the ADP amplitude was increased by raising extracellular Ca2+ concentration from 2 to 8 mM by bath application of Ba2+ (0.5-5 mM) and by intracellular injection of EGTA. This would suggest that Ca2+ itself is likely to be the charge carrier generating the ADP. Focal application of omega-conotoxin GVIA (10-30 microM) suppressed the mAHP and enhanced the ADP, whereas focal application of omega-agatoxin IVA (10-100 microM) reduced the ADP amplitude without apparent effects on the mAHP. We conclude that Ca2+ influx through omega-agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca2+ influx through omega-conotoxin GVIA-sensitive calcium channels contributes to the generation of the mAHP. Because of the selective suppression of the ADP and mAHP by omega-agatoxin IVA and omega-conotoxin GVIA, respectively, it is suggested that both calcium channels are separated geometrically in rat trigeminal motoneurons.