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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Modulation of the voltage-gated sodium- and calcium-dependent potassium channels in rat vestibular and facial nuclei after unilateral labyrinthectomy and facial nerve transsection: an in situ hybridization study.

We investigated whether the expression in the vestibular and facial nuclei of the voltage-dependent Na alpha I and Na alpha III channels and of the Ca(2+)-activated K(+)-channel subunits, small-conductance (SK) 1, SK2 and SK3, is affected by unilateral inner-ear lesion including both labyrinthectomy and transsection of the facial nerve. Specific sodium (Na alpha I, Na alpha III) and potassium (SK1, SK2, SK3) radioactive oligonucleotides were used to probe sections of rat vestibular and facial nuclei by in situ hybridization methods. The signal was detected with films or by emulsion photography. Animals were killed at various times following the lesion: 1 day, 3 days, 8 days or 30 days. In normal adult animals, mRNAs for Na alpha I, and SK1, SK2, and SK3 channels were found in several brainstem regions including the lateral, medial, superior and inferior vestibular nuclei and the facial nuclei. In contrast, there was little Na alpha III subunit mRNA anywhere in the brainstem. Following unilateral inner ear lesion in rats, the medial vestibular nuclei were probed with Na alpha I, Na alpha III, SK1, SK2 and SK3 oligonucleotide probes: autoradiography indicated no difference between the two sides, at any of the times studied. Na alpha I and SK2 mRNAs were less abundant and Na alpha III, SK1 and SK3 mRNAs were more abundant in the axotomized facial nuclei motoneurons than in controls. Removal of vestibular input did not affect the abundance of the mRNAs for the sodium- or calcium-dependent potassium channels in the deafferented vestibular nuclei. There is thus no evidence that modulation of these conductances contributes to the recovery of a normal resting discharge of the deafferented vestibular neurons and consequently to the functional recovery of the postural and oculomotor deficits observed at the acute stage. However, facial axotomy induced a long-term modulation of both Na and SK conductances mRNAs in the facial motoneurons ipsilateral to the lesion. Presumably, retrograde injury factors resulting from axotomy were able to alter durably the membrane properties and thus the excitability of the facial motoneurons.[1]

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