Ca²⁺-activated small-conductance K⁺ (SK) channels regulate neuronal excitability by coupling intracellular Ca²⁺ signals to membrane hyperpolarization. Using electrophysiological recordings from mouse hippocampal CA1 pyramidal neurons, this study demonstrates that SK channels contribute significantly to the afterhyperpolarization following action potential bursts. Blockade of SK channels reduced afterhyperpolarization, whereas M-channel inhibition had minimal effect. Additionally, SK channels were activated by Ca²⁺ influx through synaptic NMDA receptors, attenuating excitatory synaptic potentials. These findings indicate that distinct populations of SK channels couple to different Ca²⁺ sources to regulate firing and synaptic integration.
