Developmental changes in low and high voltage-activated calcium currents in acutely isolated mouse vestibular neurons.
1. The development of low voltage-activated (LVA) and high voltage-activated (HVA) calcium currents was studied in neurons acutely dissociated from mouse vestibular ganglia at embryonic stages (E)14, 15, 17 and birth using the whole-cell patch-clamp technique. 2. LVA current was present in almost all neurons tested at stages E14 to E17, although at birth this current was restricted to a few neurons. Two populations of neurons were characterized based on the amplitude of the LVA current. In the first population, LVA current densities decreased between E17 and birth by which time this current tended to disappear in most neurons. A second population of neurons with high density LVA current appeared at E17, and in this group the mean density increased during development. 3. Among HVA currents, the dihydropyridine-sensitive L-type current remained constant between E15 and birth. Over the same period, the density of N- and Q-type currents continuously increased as shown using omega-conotoxin-GVIA (N-type), and high concentrations of omega-agatoxin-IVA (Q-type). The P-type current, sensitive to low concentrations of omega-agatoxin-IVA, transiently increased between E15 and E17, and then both current density and its proportion of the global current decreased. 4. Our results reveal large modifications in the expression of voltage-dependent calcium channels during embryonic development of primary vestibular neurons. The changes in the expression of LVA current and the transient augmentation of P-type HVA current occur during a period characterized by massive neuronal growth and by the beginning of synaptogenesis. These results suggest a specific role of these currents in the ontogenesis of vestibular primary afferents.
Chambard
J M
JM
INSERM U432 Neurobiologie et Developpement du Systeme Vestibulaire, UM2, cp 089 place E. Bataillon, 34095 Montpellier Cedex 5, France.
Chabbert
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Sans
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Desmadryl
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D000818:Animals; D001464:Barium / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000502:physiology; D020864:Calcium Channels, N-Type / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004594:Electrophysiology; D015640:Ion Channel Gating / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D014722:Vestibule, Labyrinth / Q000166:cytology* / Q000187:drug effects / Q000196:embryology*; D020867:omega-Agatoxin IVA / Q000494:pharmacology; D020866:omega-Conotoxin GVIA / Q000494:pharmacology
D001464:Barium; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA