title: The involvement of Cav3.2/alpha1H T-type calcium channels in excitability of mouse embryonic primary vestibular neurones.
abstract: Ca2+ influx through voltage-gated calcium channels probably influences neuronal ontogenesis. Many developing neurones transiently express T-type/Cav3 calcium channels that contribute to their electrical activity and potentially to their morphological differentiation. Here we have characterized the electrophysiological properties and the functional role of a large T-type calcium current that is present in mouse developing primary vestibular neurones at embryonic day E17. This T-type current showed fast activation and inactivation, as well as slow deactivation kinetics. The overlap of activation and inactivation parameters produced a window current between -65 and -45 mV. Recovery from short-term inactivation was slow suggesting the presence of the Cav3.2 subunit. This T-type current was blocked by micromolar concentrations of Ni2+ and was inhibited by fast perfusion velocities in a similar fashion to recombinant Cav3.2 T-type channels expressed in HEK-293 cells. More importantly, current clamp experiments have revealed that the T-current could elicit afterdepolarization potentials during the repolarization phase of action potentials, and occasionally generate calcium spikes. Taken together, we demonstrate that the Cav3.2 subunit is likely to be the main T-type calcium channel subunit expressed in embryonic vestibular neurones and should play a key role in the excitability of these neurones during the ontogenesis of vestibular afferentation.
authors.affiliation: INSERM U583, INM, Hôpital Saint Eloi, 80 rue Augustin Fliche, 34091 Montpellier cedex 5, France.
authors.forename: Laurence
authors.initials: L
authors.lastname: Autret
authors.forename: Ilana
authors.initials: I
authors.lastname: Mechaly
authors.forename: Frédérique
authors.initials: F
authors.lastname: Scamps
authors.forename: Jean
authors.initials: J
authors.lastname: Valmier
authors.forename: Philippe
authors.initials: P
authors.lastname: Lory
authors.forename: Gilles
authors.initials: G
authors.lastname: Desmadryl
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D020747:Calcium Channels, T-Type / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D007668:Kidney / Q000166:cytology; D051379:Mice; D009475:Neurons, Afferent / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D010477:Perfusion; D011247:Pregnancy; D014162:Transfection; D014725:Vestibular Nerve / Q000166:cytology / Q000196:embryology* / Q000502:physiology*
chemical_list: C479952:CACNA1H protein, human; C504883:Cacna1h protein, mouse; D020747:Calcium Channels, T-Type; D009532:Nickel