title: Voltage-gated calcium channels in Pleurodeles oocytes: classification, modulation and functional roles.
abstract: In unfertilised Pleurodeles oocytes, two distinct types of high voltage-activated Ca2+ channels are expressed: a slowly inactivating Ca2+ channel and a transient one. The first is dihydropyridine-sensitive and is referred to as the L-type Ca2+ channel. The transient channel is highly sensitive to Ni2+. Phosphorylation through protein kinases G and A facilitates and inhibits the L-type Ca2+ channel respectively. The transient type channel is insensitive to stimulation by protein kinases (A and G). The functional expression of L-type and transient Ca2+ channels is modulated by the two maturation seasons. The transient Ca2+ currents are only observed during the resting season, while the L-type current is observed either alone during the breeding season or in association with the transient current during the resting season. Moreover, the current density of the L-type Ca2+ channel is much greater during the breeding season than the resting season. Thus, the wide distribution of L-type Ca2+ channels in Pleurodeles oocytes during the two seasons suggests that the roles of these channels may be important in the regulation of the maturation process.
authors.affiliation: Centre de Biologie Cellulaire, USTL 59655, Villeneuve d'Ascq, France. ouadid.halima@univ-lille1.fr
authors.forename: H
authors.initials: H
authors.lastname: Ouadid-Ahidouch
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D001947:Breeding; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000145:classification / Q000187:drug effects / Q000378:metabolism*; D020746:Calcium Channels, L-Type; D000242:Cyclic AMP / Q000502:physiology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D017869:Cyclic GMP-Dependent Protein Kinases / Q000378:metabolism; D004095:Dihydropyridines / Q000494:pharmacology; D004558:Electric Stimulation; D015640:Ion Channel Gating / Q000187:drug effects; D017136:Ion Transport / Q000187:drug effects; D008540:Meiosis / Q000187:drug effects; D008564:Membrane Potentials; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D009865:Oocytes / Q000187:drug effects / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology; D010766:Phosphorylation; D010999:Pleurodeles / Q000502:physiology*; D011374:Progesterone / Q000494:pharmacology; D011499:Protein Processing, Post-Translational; D012621:Seasons; D015290:Second Messenger Systems / Q000502:physiology; D020866:omega-Conotoxin GVIA
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D004095:Dihydropyridines; D010455:Peptides; D002104:Cadmium; D015124:8-Bromo Cyclic Adenosine Monophosphate; D011374:Progesterone; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; C038806:1,4-dihydropyridine; D009532:Nickel; D020866:omega-Conotoxin GVIA; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D017869:Cyclic GMP-Dependent Protein Kinases; D009543:Nifedipine; D002118:Calcium