Developmental regulation of the membrane properties of central vestibular neurons by sensory vestibular information in the mouse.
The effect of the lack of vestibular input on the membrane properties of central vestibular neurons was studied by using a strain of transgenic, vestibular-deficient mutant KCNE1(-/-) mice where the hair cells of the inner ear degenerate just after birth. Despite the absence of sensory vestibular input, their central vestibular pathways are intact. Juvenile and adult homozygous mutant have a normal resting posture, but show a constant head bobbing behaviour and display the shaker/waltzer phenotype characterized by rapid bilateral circling during locomotion. In juvenile mice, the KCNE1 mutation was associated with a strong decrease in the expression of the calcium-binding proteins calbindin, calretinin and parvalbumin within the medial vestibular nucleus (MVN) and important modifications of the membrane properties of MVN neurons. In adult mice, however, there was almost no difference between the membrane properties of MVN neurons of homozygous and control or heterozygous mutant mice, which have normal inner ear hair cells and show no behavioural symptoms. The expression levels of calbindin and calretinin were lower in adult homozygous mutant animals, but the amount of calcium-binding proteins expressed in the MVN was much greater than in juvenile mice. These data demonstrate that suppression of sensory vestibular inputs during a 'sensitive period' around birth can generate the circling/waltzing behaviour, but that this behaviour is not due to persistent abnormalities of the membrane properties of central vestibular neurons. Altogether, maturation of the membrane properties of central vestibular neurons is delayed, but not impaired by the absence of sensory vestibular information.
Eugène
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D
Laboratoire de Neurobiologie des Réseaux Sensorimoteurs, UMR 7060, CNRS-Université Paris Descartes, Paris. daniel.eugene@univ-paris5.fr
Deforges
S
S
Guimont
F
F
Idoux
E
E
Vidal
P-P
PP
Moore
L E
LE
Vibert
N
N
D000367:Age Factors; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D003423:Critical Period, Psychological; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D025802:Electric Capacitance; D018507:Gene Expression Regulation, Developmental; D018069:Hair Cells, Vestibular / Q000473:pathology* / Q000502:physiology*; D019416:Head Movements / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009924:Organ Culture Techniques; D010320:Parvalbumins / Q000235:genetics / Q000378:metabolism; D018408:Patch-Clamp Techniques; D010641:Phenotype; D024642:Potassium Channels, Voltage-Gated / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000235:genetics / Q000378:metabolism; D014726:Vestibular Nuclei / Q000254:growth & development / Q000473:pathology* / Q000502:physiology*
C576511:Calb2 protein, mouse; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins; D002614:Chelating Agents; C092068:Kcne1 protein, mouse; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D024642:Potassium Channels, Voltage-Gated; D012333:RNA, Messenger; D064030:S100 Calcium Binding Protein G; D004533:Egtazic Acid; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid