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Article type: Research Article
Authors: Zennou-Azogui, Y. | Xerri, C. | Harlay, F.
Affiliations: Laboratoire de Neurobiologie des Restaurations Fonctionnelles, URA CNRS n° 372, Université de Provence, Centre de Saint-Jérôme, Avenue Escadrille Normandie-Niemen, 13397 Marseille cedex 20, France
Note: [] Corresponding author, Tel.: (0 11 33) 91 28 84 64; Fax: (0 11 33) 91 28 86 16; e-mail: [email protected].
Abstract: In a previous study [31], we showed that Deiters' neurons ipsilateral to a vestibular neurectomy temporarily exhibit increased sensitivity to visual cues about fast movement. It was proposed that this change in the deafferented vestibular neuron response observed only during the first 3 weeks post-lesion plays an important role in the vestibular compensation process. The present study was aimed at analyzing the potential influence over the first 2 weeks post-lesion of visual motion cue deprivation (cats housed in stroboscopic light) and passive visual experience (visual information not correlated to head or body movement) on the visually induced activity of Deiters' cells. The extra-cellular response of single units was recorded during sinusoidal translation of a whole field optokinetic stimulus in six alert cats. Following the deprivation of visual motion cues, vestibular unit responses were found to be tuned to low frequencies of visual stimulation, as in intact cats, and to display a phase lag re. velocity during rapid visual stimulation. Passive visual stimulation was also found to impede the increase in neuronal sensitivity to visual input, although the cats had benefited from normal vision from the 15th day post-lesion. These results are discussed in relation to the functional implication of interactive visual experience within the early stages (sensitive period) of the vestibular compensation process.
Keywords: Alert cat, Vestibular compensation, Visual substitution, Deiters' neurons, Visuomotor decorrelation, Stroboscopic illumination, Sensitive period
DOI: 10.3233/RNN-1995-7406
Journal: Restorative Neurology and Neuroscience, vol. 7, no. 4, pp. 235-246, 1995
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