<p>Quantal synaptic transmission in vestibular endorgans is glutamatergic. Here, we investigated the vestibular phenotype of deaf <i>Vglut3</i><sup><i>−/−</i></sup> (<i>Slc17a8</i><sup><i>−/−</i></sup>) mice from the cellular to behavioral levels. In <i>Vglut3</i><sup><i>−/−</i></sup> mice, quantal synaptic transmission in utricular calyces was reduced in rate and amplitude by &gt; 95%. In vivo recordings of spontaneous activity in the vestibular nerve revealed no significant effect of VGLUT3 deletion on afferent rate and regularity, suggesting a divergent underlying mechanism compared to the silent <i>Vglut3</i><sup><i>−/−</i></sup> auditory nerve. In behavioral studies, <i>Vglut3</i><sup><i>−/−</i></sup> mice did not exhibit considerable sensorimotor or balance deficits. Type-II vestibular hair cells (VHCs) in <i>Vglut3</i><sup><i>+/+</i></sup> mice were strongly immunoreactive for VGLUT3, while type-I VHCs showed weak immunoreactivity. Collectively, these data support the view that non-quantal transmission is the predominant mode of neurotransmission between type-I VHCs and vestibular calyceal afferent neurons. We propose that non-quantal transmission is sufficient to support vestibular nerve physiology and behavioral function in <i>Vglut3</i><sup><i>−/−</i></sup> mice.</p>

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Persistence of vestibular function in the absence of glutamatergic transmission from hair cells

  • Mohona Mukhopadhyay,
  • Ruchi Modgekar,
  • Aizhen Yang-Hood,
  • Kevin K. Ohlemiller,
  • Valentin Militchin,
  • Maolei Xiao,
  • Zhijun Shen,
  • Nicholas R. Rensing,
  • Michael Wong,
  • Suh Jin Lee,
  • Rebecca P. Seal,
  • Joseph C. Holt,
  • Mark E. Warchol,
  • Susan E. Maloney,
  • Carla M. Yuede,
  • Mark A. Rutherford,
  • Tina Pangrsic

摘要

Quantal synaptic transmission in vestibular endorgans is glutamatergic. Here, we investigated the vestibular phenotype of deaf Vglut3−/− (Slc17a8−/−) mice from the cellular to behavioral levels. In Vglut3−/− mice, quantal synaptic transmission in utricular calyces was reduced in rate and amplitude by > 95%. In vivo recordings of spontaneous activity in the vestibular nerve revealed no significant effect of VGLUT3 deletion on afferent rate and regularity, suggesting a divergent underlying mechanism compared to the silent Vglut3−/− auditory nerve. In behavioral studies, Vglut3−/− mice did not exhibit considerable sensorimotor or balance deficits. Type-II vestibular hair cells (VHCs) in Vglut3+/+ mice were strongly immunoreactive for VGLUT3, while type-I VHCs showed weak immunoreactivity. Collectively, these data support the view that non-quantal transmission is the predominant mode of neurotransmission between type-I VHCs and vestibular calyceal afferent neurons. We propose that non-quantal transmission is sufficient to support vestibular nerve physiology and behavioral function in Vglut3−/− mice.