Population
HEK 293 cells stably expressing hSK1 and rSK2 channels
Design
Preclinical
Authors
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Apamin/scyllatoxin show insufficient SK1/SK2 selectivity in mammalian cells; challenges hSK1 mediation of apamin-insensitive neuronal AHP and leaves mechanism open.
The pharmacological separation between SK channel subtypes expressed in mammalian cells is too small to support the notion that apamin-insensitive afterhyperpolarization of neurones is mediated by hSK1.
Strøbæk et al. (2000) studied this question.
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