Post‐inhibitory excitation and inhibition in layer V pyramidal neurones from cat sensorimotor cortex.

The effect of conditioning pre-pulses on repetitive firing evoked by intracellular current injection was studied in layer V pyramidal neurones in a brain slice preparation of cat sensorimotor cortex. Most cells displayed spike frequency adaptation (monotonic decline of firing rate to a tonic value) for several hundred milliseconds when depolarized from resting potential, but the cells differed in their response when pre-pulses to other potentials were employed. In one group of cells, the initial firing rate increased as the pre-pulse potential was made more negative (post-hyperpolarization excitation). Adaptation was abolished by depolarizing prepulses. In a second group, the initial firing rate decreased as the pre-pulse potential was made more negative (post-hyperpolarization inhibition). Hyperpolarizing pre-pulses caused the initial firing to fall below and accelerate to the tonic rate over a period of several seconds. A third group displayed a mixture of these two responses: the first three to seven interspike intervals became progressively shorter and subsequent intervals became progressively longer as the conditioning pre-pulse was made more negative (post-hyperpolarization mixed response). 2. Cells were filled with horseradish peroxidase or biocytin after the effect of pre-pulses was determined. All cells whose firing patterns were altered by pre-pulses were large layer V pyramidal neurones. Cells showing post-hyperpolarization excitation or a mixed response had tap root dendrites, fewer spines on the apical dendrite and larger soma diameters than cells showing post-hyperpolarization inhibition. 3. Other electrophysiological parameters varied systematically with the response to conditioning pre-pulses. Both the mean action potential duration and the input resistance of cells showing post-hyperpolarization excitation were about half the values measured in cells showing post-hyperpolarization inhibition. Values were intermediate in cells showing a post-hyperpolarization mixed response. The after-hyperpolarization following a single evoked action potential was 20% briefer in cells showing post-hyperpolarization excitation compared to those showing inhibition. 4. Membrane current measured during voltage clamp suggested that two ionic mechanisms accounted for the three response patterns. Post-hyperpolarization excitation was caused by deactivation of the inward rectifier current (Ih). Selective reduction of Ih with extracellular caesium diminished post-hyperpolarization excitation, whereas blockade of calcium influx had no effect. Post-hyperpolarization inhibition was caused by enhanced activation of a slowly inactivating potassium current. Selective reduction of this current with 4-aminopyridine diminished the post-hyperpolarization inhibition. 5. Chord conductances underlying both Ih and the slow-transient potassium current were measured and divided by leakage conductance to control for differences in cell size.(ABSTRACT TRUNCATED AT 400 WORDS)