Calcium-dependent potassium currents in neurons from cat sensorimotor cortex

J Neurophysiol. 1992 Jan;67(1):216-26. doi: 10.1152/jn.1992.67.1.216.


1. Ca(2+)-dependent K+ currents were studied in large pyramidal neurons (Betz cells) from layer V of cat sensorimotor cortex by use of an in vitro brain slice and single microelectrode voltage clamp. The Ca(2+)-dependent outward current was taken as the difference current obtained before and after blockade of Ca2+ influx. During step depolarizations in the presence of tetrodotoxin (TTX), this current exhibited a fast onset of variable amplitude and a prominent slowly developing component. 2. The Ca(2+)-dependent outward current first appeared when membrane potential was stepped positive to -40 mV. Downsteps from a holding potential of -40 mV revealed little or no time-, voltage-, or Ca(2+)-dependent current. When membrane potential was stepped positive to -40 mV, a prolonged Ca(2+)-dependent outward tail current followed repolarization. The decay of this tail current at -40 mV was best described by a single exponential function having a time constant of 275 +/- 75 (SD) ms. The tail current reversed at 96 +/- 5 mV in 3 mM extracellular K+ concentration ([K+]o) and at more positive potentials when [K+]o was raised, suggesting that it was carried predominantly by K+. 3. The Ca(2+)-dependent K+ current consisted of two pharmacologically separable components. The slowly developing current was insensitive to 1 mM tetraethylammonium (TEA), but a substantial portion was reduced by 100 nM apamin. Most of the remaining current was blocked by the addition of isoproterenol (20-50 microM) or muscarine (10-20 microM). 4. The time courses of the apamin- and transmitter-sensitive components were similar when activated by step depolarizations in voltage clamp, but they were quite different when activated by a train of action potentials. Applying the voltage clamp at the end of a train of 90 spikes (evoked at 100-200 Hz) resulted in an Ca(2+)-dependent K+ current with a prominent rapidly decaying portion (time constant approximately 50 ms at -64 mV) and a smaller slowly decaying portion (time constant approximately 500 ms at -64 mV). The rapidly decaying portion was blocked by apamin (50-200 nM), and the slowly decaying portion was blocked by isoproterenol (20-50 microM). 5. When recorded with microelectrodes containing 2 mM dimethyl-bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (dimethyl-BAPTA), which causes prolonged afterhyperpolarizations, the Ca(2+)-dependent K+ current evoked by step depolarizations had an extremely slow onset and decay. The current recorded after a train of evoked spikes had a similar slow decay.(ABSTRACT TRUNCATED AT 400 WORDS)

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apamin / pharmacology
  • Calcium / physiology*
  • Calcium Channels / drug effects
  • Cats
  • Egtazic Acid / analogs & derivatives
  • Egtazic Acid / pharmacology
  • In Vitro Techniques
  • Isoproterenol / pharmacology
  • Membrane Potentials / drug effects
  • Microelectrodes
  • Motor Cortex / cytology
  • Motor Cortex / metabolism
  • Motor Cortex / physiology*
  • Neurons / drug effects
  • Neurons / physiology*
  • Potassium Channels / drug effects
  • Potassium Channels / physiology*
  • Pyramidal Tracts / cytology
  • Pyramidal Tracts / drug effects
  • Tetraethylammonium Compounds / pharmacology
  • Tetrodotoxin / pharmacology


  • Calcium Channels
  • Potassium Channels
  • Tetraethylammonium Compounds
  • Apamin
  • Tetrodotoxin
  • Egtazic Acid
  • 5,5'-dimethyl-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate
  • Isoproterenol
  • Calcium