Changes in neuronal activity often trigger compensatory mechanisms aimed at regulating network activity homeostatically. Here we have identified and characterized a novel form of compensatory short‐term plasticity of membrane excitability, which develops early after the eye‐opening period in rats (P16–19 days) but not before that developmental stage (P9–12 days old). Holding the membrane potential of CA1 neurons right below the firing threshold from 15 s to several minutes induced a potentiation of the repolarizing phase of the action potentials that contributed to a decrease in the firing rate of CA1 pyramidal neurons in vitro. Furthermore, the mechanism for inducing of this plasticity required the action of intracellular calcium entering through T‐type calcium channels. This increase in calcium subsequently activated the calcium‐sensor K+ channel interacting protein 3 which led to the increase of an A‐type potassium current. These results suggest that calcium modulation of somatic A‐current represents a new form of homeostatic regulation that provides CA1 pyramidal neurons with the ability to preserve their firing abilities in response to membrane potential variations on a scale from tens of seconds to several minutes. This article is protected by copyright. All rights reserved