Slow clamp currents were recorded from CA1 and CA3 pyramidal neurones in slices of guinea‐pig hippocampus maintained in vitro, using a single micro‐electrode sample‐and‐hold technique. Depolarizing voltage commands evoked a time‐ and voltage‐dependent outward current which was suppressed by removing external Ca or by adding Cd (0.5 mM) or Mn (5 mM). This Ca‐dependent current (Ic) was not reduced by muscarinic agonists (unlike IM) but was greatly reduced by 5‐20 mM‐tetraethylammonium (TEA). Repolarizing IC tail currents reversed at ‐73 +/‐ 5 mV in 3 mM‐K solution. The reversal potential became about 30 mV more positive on raising (K)o to 15 mM. No clear change in current amplitude or tail‐current reversal potential occurred on adding Cs (2 mM), reducing (Cl)o from 128 to 10 mM, or replacing external Na with Tris. The underlying conductance GC was activated at membrane potentials positive to ‐45 mV. At ‐32 mV GC showed an approximately exponential increase with time, with a time constant of approximately 0.6 sec at 26 degrees C. Repolarizing tail currents declined exponentially with time, the time constant becoming shorter with increasing negative post‐pulse potentials. When the clamp was switched off at the end of a depolarizing command of sufficient amplitude and duration to activate IC, a membrane hyperpolarization to ‐73 mV ensued, of similar amplitude and decay time to that following spontaneous action potentials. It is concluded that the clamp current observed in these experiments is probably the Ca‐activated K current thought to contribute to the post‐activation after‐hyperpolarization in hippocampal neurones.
The Journal of Physiology – Wiley
Published: Apr 1, 1983
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