IONIC MECHANISMS UNDERLYING THE DEPOLARIZING AND HYPERPOLARIZING AFTERPOTENTIALS OF SINGLE SPIKE IN GUINEA-PIG CINGULATE CORTICAL-NEURONS

Intracellular recordings and hybrid single-microelectrode voltage-clam p techniques were used to study the ionic mechanisms underlying the af terdepolarization and the subsequent slow afterhyperpolarization that followed a single action potential in layers V/VI neurons of the guine a-pig anterior cingulate cortex in in vitro slices. Both the afterdepo larization and afterhyperpolarization were markedly suppressed in size by addition of Co2+ or Cd2+, reduction in extracellular Ca2+, and int racellular EGTA injection. On the other hand, elevation of extracellul ar Ca2+ concentration augmented the amplitudes of the afterpotentials. The afterdepolarization amplitude was selectively depressed by the st ilbene derivatives, amido-4'-isothiocyanatostilbene-2,2'-disulphonate, disodium 3H2O, and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic aci d, disodium salt. Reduction in external Cl- and intracellular Cl- inje ction enhanced the afterdepolarization amplitude without affecting the afterhyperpolarization. The null potentials for the afterdepolarizati ons recorded with K acetate- and Cs acetate-electrodes were -68 and -6 3 mV, respectively. The slope of the null potential obtained with K ac etate electrodes or Cs acetate electrodes was 49 and 53 mV, respective ly, per log unit of the external Cl- concentration. Reduction in exter nal K+ markedly depressed the afterdepolarization and augmented the af terhyperpolarization in size, whereas rise in external K+ markedly aug mented the afterdepolarization and depressed the afterhyperpolarizatio n. The null potential for the afterhyperpolarization recorded with K a cetate electrodes was -94 mV. The slope of the null potential was 57 m V per log unit of the external K+ concentration. Reduction in extracel lular Na+ concentration slightly depressed both the amplitudes of the afterdepolarization and afterhyperpolarization. A hybrid voltage-clamp analysis revealed a slow decaying inward current and a subsequent out ward current that followed an action potential. Both the amplitudes of the inward current corresponding to afterdepolarization and the outwa rd current corresponding to afterhyperpolarization were suppressed by addition of Co2+. Reduction in extracellular Cl- concentration augment ed the inward current amplitude without significantly affecting the ou tward current. These results indicate that the afterdepolarization is mainly due to an increase in a Ca2+-activated Cl- conductance, while t he afterhyperpolarization is mainly generated by an activation of Ca2-mediated K+ conductance.