BK channels paradoxically act as positive feedback regulators of action potential-driven Ca2+ entry in pituitary somatotrophs by promoting plateau bursting.
May inform pituitary cell excitability models; leaves open translation to human neuroendocrine function or BK-targeted therapies.
Activation of high-conductance Ca(2+)-activated K(+) (BK) channels normally limits action potential duration and the associated voltage-gated Ca(2+) entry by facilitating membrane repolarization. Here we report that BK channel activation in rat pituitary somatotrophs prolongs membrane depolarization, leading to the generation of plateau-bursting activity and facilitated Ca(2+) entry. Such a paradoxical role of BK channels is determined by their rapid activation by domain Ca(2+), which truncates the action potential amplitude and thereby limits the participation of delayed rectifying K(+) channels during membrane repolarization. Conversely, pituitary gonadotrophs express relatively few BK channels and fire single spikes with a low capacity to promote Ca(2+) entry, whereas an elevation in BK current expression in a gonadotroph model system leads to the generation of plateau-bursting activity and high-amplitude Ca(2+) transients.
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Goor et al. (2001) studied this question.
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