title: Vasoactive intestinal peptide (VIP) may reduce the removal rate of cytosolic Ca2+ after transient elevations in clonal rat lactotrophs.
abstract: The prolactin-producing rat anterior pituitary GH4C1 cells possess Ca2+-activated K channels which are activated by physiological elevations of the cytosolic Ca2+ concentration even at membrane potentials more negative than the normal level of about -50 mV. Whole-cell current recordings showed a marked outward tail current following depolarizing voltage steps to 0 mV from a holding potential close to the normal membrane potential. The half-time of this tail current was about 1.3 s after a 4-s depolarization step. The GH4C1 cells also possess voltage-activated Ca channels, and we conclude that this tail current is a Ca2+-activated K+ current for the following reasons: (1) The reversal potential for the tail current was close to the K+ equilibrium potential for a range of transmembrane K+ gradients. (2) The tail current was blocked by a Ca2+ antagonist, and the voltage dependence of this current closely mirrored the voltage dependence of the isolated Ca2+ current. The time-course of the decline of the tail current thus reflects the removal rate of the Ca2+ entering the cytosol through voltage-dependent Ca channels during the depolarizing voltage step. VIP stimulates prolactin secretion from GH4C1 cells, and this peptide prolonged the half-time of the tail current by about 47% in 63% of the cells. This indicates that VIP may prolong the transient cytosolic Ca2+ elevations following the action potentials in these cells. Such a mechanism might be an important factor for the control of the cytosolic Ca2+ level, and hence hormone secretion.
authors.affiliation: Department of Biology, University of Oslo, Norway.
authors.forename: O
authors.initials: O
authors.lastname: Sand
authors.forename: B
authors.initials: B
authors.lastname: Chen
authors.forename: Q
authors.initials: Q
authors.lastname: Li
authors.forename: H E
authors.initials: HE
authors.lastname: Karlsen
authors.forename: T
authors.initials: T
authors.lastname: Bjøro
authors.forename: E
authors.initials: E
authors.lastname: Haug
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002999:Clone Cells; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism*; D005071:Evoked Potentials / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology*
chemical_list: D015221:Potassium Channels; D014660:Vasoactive Intestinal Peptide; D011388:Prolactin; D000242:Cyclic AMP; D002118:Calcium