Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 93, Issue 2, Pages 643-655Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00160.2004
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Funding
- NIDCD NIH HHS [K23 DC-00196, R01 DC-02390, P30 DC-05211, R03 DC-005700] Funding Source: Medline
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Gentamicin is toxic to vestibular hair cells, but its effects on vestibular afferents have not been defined. We treated anesthetized chinchillas with one injection of gentamicin (26.7 mg/ml) into the middle ear and made extracellular recordings from afferents after 5-25 ( early) or 90-115 days ( late). The relative proportions of regular, intermediate, and irregular afferents did not change after treatment. The spontaneous firing rate of regular afferents was lower (P <0.001) on the treated side (early: 44.3 +/- 16.3; late: 33.9 +/- 13.2 spikes . s(-1)) than on the untreated side (54.9 +/- 16.8 spikes . s(-1)). Spontaneous rates of irregular and intermediate afferents did not change. The majority of treated afferents did not measurably respond to tilt or rotation (82% in the early group, 76% in the late group). Those that did respond had abnormally low sensitivities (P < 0.001). Treated canal units that responded to rotation had mean sensitivities only 5-7% of the values for untreated canal afferents. Treated otolith afferents had mean sensitivities 23-28% of the values for untreated otolith units. Sensitivity to externally applied galvanic currents was unaffected for all afferents. Intratympanic gentamicin treatment reduced the histological density of all hair cells by 57% (P = 0.04). The density of hair cells with calyx endings was reduced by 99% (P = 0.03), although some remaining hair cells had other features suggestive of type I morphology. Type II hair cell density was not significantly reduced. These findings suggest that a single intratympanic gentamicin injection causes partial damage and loss of vestibular hair cells, particularly type I hair cells or their calyceal afferent endings, does not damage the afferent spike initiation zones, and preserves enough hair cell synaptic activity to drive the spontaneous activity of vestibular afferents.
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