Abstract
Catecholaminergic inputs into the inner ear originate from the superior cervical ganglion (SCG). Alpha-adrenergic receptors (ARs) are located around the spiral modular artery and are involved in vasocontraction and cochlear blood flow. Beta 1-ARs in the strial marginal cells and vestibular dark cells have a regulatory role on endolymph production. Beta 2-ARs in the endolymphatic sac also control endolymph absorption. Therefore, stress-induced sympathetic nerve hyperactivity might promote adrenergic effects on the inner ear, resulting in the onset of sudden deafness and/or Meniere's disease. Beta 2-ARs show significant long-lasting up-regulation not only in the affected side of the vestibular ganglion (VG) but also in the healthy side, when a great imbalance exists between bilateral vestibular nuclei (VN) activities. Bilateral simultaneous labyrinthectomies have no significant effects on beta 2-AR expression in VG. This finding suggests that beta 2-ARs in the VG could play a neuro-plastic role in vestibular compensation. Further studies are needed to elucidate the molecular mechanisms in catecholamine and vestibular periphery-mediated vertigo.
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