Abstract
CA1 and CA3 neurons in transverse slices of guinea pig hippocampus were voltage clamped through a single micro-electrode, and perfused with Krebs solution containing 0.5 .mu.M-tetrodotoxin and 10 .mu.M-tetraethylammonium at (normally) 24-26.degree. C. Slow inward currents of .ltoreq. 0.5 nA were recorded during depolarizing voltage commands to membrane potentials positive to between -40 and -30 mV. These currents peaked at 100-300 ms after the onset of the depolarizing command, then subsequently declined during continuing depolarization. This decline could be ascribed to a developing outward current since repolarizing inward current tails showed no diminution up to 700 ms. No clear evidence for time-dependent inactivation of the inward current could be obtained. A persistent component of inward current could be detected when the membrane potential was maintained above the inward current threshold, such that small hyperpolarizing commands induced an outward relaxation and large hyperpolarizations produced an inward tail current. The inward current was depressed by removing external Ca, or by adding 0.2-0.5 mM-Cd, or 0.1 mM-verapamil, and was increased by adding 1 mm-Ba. A possible role for this persistent inward current in generating the low membrane depolarization underlying burst discharges in these neurons is discussed. In some neurons (primarily CA1), an additional fast spike-like current was recorded, which was blocked by Cd or Mn and depressed by a depolarizing pre-pulse. This was a manifestation of the previously-reported dendritic Ca spike.