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Small-conductance Ca 2+ -activated K +  (SK) and large-conductance voltage- and Ca 2+ -activated K +  (BK) channels are Ca 2+ -activated K +  channels that control action potential firing in diverse neurons in the brain. In cartwheel cells of the dorsal cochlear nucleus, blockade of either channel type leads to excessive production of spike bursts. In the same cells, P/Q-type Ca 2+  channels in plasma membrane and ryanodine receptors in endoplasmic reticulum supply Ca 2+  to BK channels through Ca 2+  nanodomain signaling. In this study, voltage-clamp experiments were performed in cartwheel cells in mouse brain slices to examine the Ca 2+  signaling pathways underlying activation of SK channels. As with BK channels, SK channels required the activity of P/Q-type Ca 2+  channels. However, this signaling occurred across Ca 2+  micro- rather than nanodomain distances and was independent of Ca 2+  release from endoplasmic reticulum. These differential modes of activation may lead to distinct time courses of the two K +  currents and therefore control excitability of auditory neurons across different timescales.    NEW &amp; NOTEWORTHY This study has shown for the first time that in cartwheel cells of the dorsal cochlear nucleus, small-conductance Ca 2+ -activated K +  (SK) channels were triggered by the activation of P/Q-type Ca 2+  channels in which SK–P/Q-type coupling is mediated within the Ca 2+  microdomains (loose coupling). Although Ca 2+ -induced Ca 2+  release is able to activate large-conductance voltage- and Ca 2+ -activated K +  (BK) channels in cartwheel cells, it did not contribute to SK activation.

Loose coupling between SK and P/Q-type Ca2+ channels in cartwheel cells of the dorsal cochlear nucleus

Loose coupling between SK and P/Q-type Ca²⁺ channels in cartwheel cells of the dorsal cochlear nucleus