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Sylvain Bartolami

Researcher at University of Montpellier

Publications -  12
Citations -  307

Sylvain Bartolami is an academic researcher from University of Montpellier. The author has contributed to research in topics: Inner ear & Spinal cord injury. The author has an hindex of 9, co-authored 12 publications receiving 264 citations. Previous affiliations of Sylvain Bartolami include French Institute of Health and Medical Research.

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Appearance and distribution of the 275 kD hair-cell antigen during development of the avian inner ear.

TL;DR: Serial section analysis indicates that expression of the HCA is always limited to areas of the epithelium where nerve fibres are found, although the delay between the onset of innervation and the onsetof HCA expression varies from one region of the otocyst to another.
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Optimal myelin elongation relies on YAP activation by axonal growth and inhibition by Crb3/Hippo pathway

TL;DR: Dystrophic Dy2j/2j mice mimicking human peripheral neuropathy with reduced internodal lengths have decreased nuclear YAP which, when corrected, leads to longer internodes, showing a novel mechanism controlling myelin growth and nerve conduction, and provide a molecular ground for disease with short myelin segments.
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Pre- and postsynaptic M3 muscarinic receptor mRNAs in the rodent peripheral auditory system

TL;DR: The results suggest that the M3 receptor-induced inositol phosphate formation described in previous studies takes place in both postsynaptic (SGNs, OHCs) and presynaptic components of efferent cochlear synapses, and in cells that are not contacted by efferents in the adult cochlea (IHCs).
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Inhibition of calcium-dependent motility of cochlear outer hair cells by the protein kinase inhibitor, ML-9.

TL;DR: The data support the hypothesis that protein kinase activity regulates calcium-dependent processes that affect shape changes of outer hair cells, and are consistent with the involvement of the calcium/calmodulin-dependent enzyme, myosin light chain kinase, a known target of ML-9, but do not preclude the possibility of another intracellular target forML-9.