| First Author | Hübner PP | Year | 2017 |
| Journal | J Neurophysiol | Volume | 117 |
| Issue | 4 | Pages | 1553-1568 |
| PubMed ID | 28077670 | Mgi Jnum | J:274476 |
| Mgi Id | MGI:6295233 | Doi | 10.1152/jn.01049.2015 |
| Citation | Hubner PP, et al. (2017) The mammalian efferent vestibular system plays a crucial role in vestibulo-ocular reflex compensation after unilateral labyrinthectomy. J Neurophysiol 117(4):1553-1568 |
| abstractText | The alpha9-nicotinic acetylcholine receptor (alpha9-nAChR) subunit is expressed in the vestibular and auditory periphery, and its loss of function could compromise peripheral input from the predominantly cholinergic efferent vestibular system (EVS). A recent study has shown that alpha9-nAChRs play an important role in short-term vestibulo-ocular reflex (VOR) adaptation. We hypothesize that alpha9-nAChRs could also be important for other forms of vestibular plasticity, such as that needed for VOR recovery after vestibular organ injury. We measured the efficacy of VOR compensation in alpha9 knockout mice. These mice have deletion of most of the gene (chrna9) encoding the nAChR and thereby lack alpha9-nAChRs. We measured the VOR gain (eye velocity/head velocity) in 20 alpha9 knockout mice and 16 cba129 controls. We measured the sinusoidal (0.2-10 Hz, 20-100 degrees /s) and transient (1,500-6,000 degrees /s(2)) VOR in complete darkness before (baseline) unilateral labyrinthectomy (UL) and then 1, 5, and 28 days after UL. On day 1 after UL, cba129 mice retained ~50% of their initial function for contralesional rotations, whereas alpha9 knockout mice only retained ~20%. After 28 days, alpha9 knockout mice had ~50% lower gain for both ipsilesional and contralesional rotations compared with cba129 mice. Cba129 mice regained ~75% of their baseline function for ipsilesional and ~90% for contralesional rotations. In contrast, alpha9 knockout mice only regained ~30% and ~50% function, respectively, leaving the VOR severely impaired for rotations in both directions. Our results show that loss of alpha9-nAChRs severely affects VOR compensation, suggesting that complimentary central and peripheral EVS-mediated adaptive mechanisms might be affected by this loss.NEW & NOTEWORTHY Loss of the alpha9-nicotinic acetylcholine receptor (alpha9-nAChR) subunit utilized by the efferent vestibular system (EVS) has been shown to significantly affect vestibulo-ocular reflex (VOR) adaptation. In our present study we have shown that loss of alpha9-nAChRs also affects VOR compensation, suggesting that the mammalian EVS plays an important role in vestibular plasticity, in general, and that VOR compensation is a more distributed process than previously thought, relying on both central and peripheral changes. |
