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1 Geriatric Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan; Cardiovscular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan
2 Geriatric Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan
3 Cardiovscular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan
4 Integrative Brain Science, Kyoto University Graduate School of Medicine, Kyoto, Japan
* To whom correspondence should be addressed. E-mail: f50207{at}sakura.kudpc.kyoto-u.ac.jp.
Cooperative regulation of inosiol-1,4,5-trisphosphate receptors (IP3Rs) by Ca2+ and IP3 has been increasingly recognized, though its functional significance is not clear. The present experiments first confirmed that depolarization-induced Ca2+ influx triggers an outward current in visual cortex pyramidal cells in normal medium, which was mediated by apamin-sensitive, small conductance Ca2+-dependent K+ channels (SK channels). With IP3-mobilizing neurotransmitters bath-applied, a delayed outward current was evoked in addition to the initial outward current, and was mediated again by SK channels. Calcium turnover underlying this biphasic SK channel activation was investigated. By voltage-clamp recording, Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs) was shown to be responsible for activating the initial SK current, whereas the IP3R blocker heparin abolished the delayed component. High-speed Ca2+ imaging revealed that a biphasic Ca2+ elevation indeed underlay this dual activation of SK channels. The first Ca2+ elevation originated from VDCCs, whereas the delayed phase was attributed to calcium release from IP3Rs. Such enhanced SK currents, activated dually by incoming and released calcium, were shown to intensify spike frequency adaptation. We propose that spike-induced calcium release from IP3Rs leads to SK channel activation, thereby fine-tuning membrane excitability in central neurons.
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