title: Paradoxical role of large-conductance calcium-activated K+ (BK) channels in controlling action potential-driven Ca2+ entry in anterior pituitary cells.
abstract: 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.
authors.affiliation: Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510, USA.
authors.forename: F
authors.initials: F
authors.lastname: Van Goor
authors.forename: Y X
authors.initials: YX
authors.lastname: Li
authors.forename: S S
authors.initials: SS
authors.lastname: Stojilkovic
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000493:pharmacokinetics; D015220:Calcium Channels / Q000378:metabolism; D002451:Cell Compartmentation / Q000502:physiology; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D005246:Feedback / Q000502:physiology; D005260:Female; D006062:Gonadotropins / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology; D007211:Indoles / Q000494:pharmacology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D051036:Large-Conductance Calcium-Activated Potassium Channels; D008954:Models, Biological; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D015220:Calcium Channels; D002614:Chelating Agents; D006062:Gonadotropins; D007211:Indoles; D051036:Large-Conductance Calcium-Activated Potassium Channels; D010455:Peptides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; C048220:paxilline; D004533:Egtazic Acid; D011189:Potassium Chloride; C064719:iberiotoxin; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D002118:Calcium