Kv1 channels control spike threshold dynamics and spike timing in cortical pyramidal neurones

Non‐Technical Summary  Spiking neurones generate action potentials when the transmembrane voltage difference near the spike generating zone reaches a threshold level. Above the threshold, the inward sodium current exceeds the outward potassium current, causing the rapid upstroke of the action potential. In many neurones, including cortical pyramidal cells, the threshold is not constant but responds to a change in voltage with a short delay. The functional effect is equivalent to high‐pass filtering of the voltage response, and a major benefit is enhanced spike timing precision. Two mechanisms that may contribute to a dynamic spike threshold are sodium channel inactivation and potassium channel activation, both caused by a rise in voltage. We found that blocking low‐threshold Kv1 potassium channels greatly reduced threshold changes in pyramidal neurones located in layer 2–3 of the rat motor cortex. Studies using noise stimulation showed that blocking Kv1 impaired the ability of these cells to encode fast components of the input signal with precisely timed spikes. These results demonstrate a key role of Kv1 in cortical spike timing, with possible implications for information coding as well as pathological hypersynchronous discharges in epilepsy.