title: Regulation of Ca2+-activated nonselective cationic currents in rat pituitary GH3 cells: involvement in L-type Ca2+ current.
abstract: Ionic currents were investigated by a patch clamp technique in a clonal strain of pituitary (GH3) cells, using the whole cell configuration with Cs+ internal solution. Depolarizing pulses positive to 0 mV from a holding potential of -50 mV activated the voltage-dependent L-type Ca2+ current (ICa,L) and late outward current. Upon repolarization to the holding potential, a slowly decaying inward tail current was also observed. This inward tail current upon repolarization following a depolarizing pulse was found to be enhanced by Bay K 8644, but blocked by nifedipine or tetrandrine. This current was eliminated by Ba2+ replacement of external Ca2+ as the charge carrier through Ca2+ channels, removal of Ca2+ from the bath solution, or buffering intracellular Ca2+ with EGTA (10 mM). The reversal potential of inward tail current was approximately -25 mV. When intracellular Cl- was changed, the reversal potential of the Ca2+-activated currents was not shifted. Thus, this current is elicited by depolarizing pulses that activate ICa,L and allow Ca2+ influx, and is referred to as Ca2+-activated nonselective cationic current (ICAN). Without including EGTA in the patch pipette, the slowly decaying inward current underlying the long-lasting depolarizing potential after Ca2+ spike was also observed with a hybrid current-voltage protocol. Thus, the present studies clearly indicate that Ca2+-activated nonselective cationic channels are expressed in GH3 cells, and can be elicited by the depolarizing stimuli that lead to the activation of ICa,L.
authors.affiliation: Department of Medical Education and Research, Veterans General Hospital-Kaohsiung, No. 386, Ta-Chung 1st Rd., Kaohsiung City, Taiwan. snw@isca.vghks.gov.tw
authors.forename: S N
authors.initials: SN
authors.lastname: Wu
authors.forename: H F
authors.initials: HF
authors.lastname: Li
authors.forename: C R
authors.initials: CR
authors.lastname: Jan
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010903:Pituitary Gland, Anterior / Q000502:physiology*; D051381:Rats; D014407:Tumor Cells, Cultured
chemical_list: D017609:Barium Compounds; D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002712:Chlorides; C024986:barium chloride; D002586:Cesium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine