Учебники / Hair Cell Regeneration, Repair, and Protection Salvi 2008

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2. Changes in Absolute Sensitivity

There have been principally two ways to damage auditory sensory cells with resulting changes in sensory function: acoustic trauma and administration of ototoxic drugs. The two approaches typically lead to different patterns of hair cell damage and loss and different patterns of hair cell regeneration and functional recovery (Saunders et al. 1995; Salvi et al. 1998; Cotanche 1999; Smolders 1999). Here, we discuss the extents and time courses of hearing loss and functional recovery to these two types of peripheral auditory system trauma in birds.

2.1 Acoustic Overexposure

Morphological assessment of hair cell loss and regeneration after acoustic trauma has shown that acoustic overstimulation generally results in the loss of some, but not all, hair cells in a specific location on the basilar papilla, depending on the type, intensity, and duration of the acoustic trauma (reviewed in Cotanche 1999).

Temporary hearing loss in birds after acoustic overexposure, first described in budgerigars (Melopsittacus undulatus), revealed some differences between birds and mammals (Saunders and Dooling 1974; Dooling 1980). Budgerigars exposed to 1/3 octave bands of noise centered at 2 kHz for 72 hours at levels of 76–106 dB sound pressure level (SPL) showed maximum hearing losses at 2 kHz, and the threshold shift ranged from 10 to 40 dB depending on the level of the exposure. A permanent threshold shift was observed only with the 106-dB exposure, suggesting that birds, compared to mammals, are more resistant to damage from noise (Dooling 1980). Temporary threshold shifts in these birds were also of a shorter duration than typically seen in mammals and were also restricted to a narrower range of frequencies (e.g., Luz and Hodge 1971; Price 1979; Dooling 1980; Henderson and Hamernik 1986). In addition to showing little spread across frequencies, in budgerigars the maximum threshold shift occurred at higher frequencies than the exposure frequency. Hashino and colleagues (1988) extended these bird–mammal differences to impulse noise exposures. Two 169-dB SPL impulse noises produced by pistols caused more low-frequency than high-frequency hearing loss with the return to preexposure hearing levels occurring at a faster rate for high than for low frequencies. These results are unique and intriguing, and their confirmation could provide insight into the functioning of the avian ear.

Japanese quail (Coturnix coturnix) exposed to a 1.5-kHz octave band noise at 116 dB SPL for 4 hours showed elevated thresholds for pure tones up to 50 dB immediately after exposure (Niemiec et al. 1994). Thresholds were most severely affected at frequencies of 1.0 kHz and above, although there was considerable variation among subjects. Thresholds improved rapidly within the first week after exposure, recovering to preexposure levels by 8–10 days. Damaged hair cells were still observed up to 2 weeks postexposure but not by 5 weeks postexposure. Similar patterns of threshold shifts and recoveries were seen after repeated

exposures to noise, although recovery times increased with increasing numbers of exposures. Interestingly, Niemiec et al. (1994) found that structural abnormalities (elongated stereocilia, supporting cell expansion, and stress links between hair cells) remained for at least 4 weeks after pure tone sensitivity had recovered. They suggested that while these abnormalities may not influence absolute threshold sensitivity, they may be involved in other aspects of functional hearing. Other investigators have suggested that lingering structural abnormalities within the tectorial membrane (lack of upper fibrous layer) may be related to incomplete recovery of other aspects of auditory function such as frequency resolution (Salvi et al. 1998; Lifshitz et al. 2004). While neural correlates of frequency resolution tend to corroborate poorer frequency resolving capacity after acoustic trauma and hair cell regeneration, corresponding behavioral studies are still lacking. Behavioral studies of frequency resolution after hair cell regeneration following ototoxic insult have been performed and are described later in this chapter.

Ryals and colleagues (1999b) found that the amount of hearing loss and the time course of recovery varied considerably among different species of adult (sexually mature) birds even when exposure conditions and test conditions were identical. In their study, quail and budgerigars were exposed to intense pure tones centered in their region of best hearing at 112–118 dB SPL for 12 hours. Quail showed much greater susceptibility to acoustic trauma than did budgerigars, with significantly larger threshold shifts and hair cell loss. Quail showed a threshold shift of 70 dB at 2.86 kHz 1 day after overexposure. Thresholds for the quail remained virtually unchanged for 8–9 days postexposure, and then began to improve by about 2 dB/day until day 30. Quail experienced a permanent threshold shift of approximately 20 dB, which remained even when tested 1 year after exposure. Budgerigars exhibited a threshold shift of about 35–40 dB at 0.5 days after exposure, but showed a much faster recovery than quail. By 3 days postexposure, budgerigars’ thresholds had improved to within 10 dB of normal. Chickens exposed to a 120-dB pure tone at 525 Hz for 48 hours (Saunders et al. 1995) showed similar initial threshold shifts and rates of recovery as the budgerigars. CAP measurements in pigeons exposed to a 142-dB pure tone at 700 Hz for 1 hour (Ding-Pfennigdorff et al. 1998) showed intermediate threshold shifts between the quail and the budgerigars and chickens.

In a more comprehensive study, budgerigars, canaries (Serinus canaria), and zebra finches (Taeniopygia guttata) were exposed to a bandpass noise (2–6 kHz) at 120 dB SPL for 24 hours (Ryals et al. 1999b). These birds showed thresholds at 1.0 kHz that were elevated by 10–30 dB and that improved to within normal limits by about 10 days postexposure in all three species. At 2.86 kHz, the center of the exposure band, budgerigars, canaries, and zebra finches showed a 50-dB threshold shift. Recovery began immediately afterward for canaries and finches, and threshold improved to within 10 dB of normal by about 30 days postexposure. In budgerigars, threshold recovery did not begin until 10 days postexposure. By 50 days postexposure, thresholds recovered to about 20 dB above normal, and no

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further improvement occurred by 70 days, at which point the loss was assumed to be permanent. Overall, results showed a significantly more rapid recovery in canaries and zebra finches than in budgerigars. Histological analysis in all of these birds quantified hair cell loss and recovery in the region of damage before, during, and after threshold recovery. In general, the more severe the initial degree of hair cell loss (width of damage and decrease in hair cell number) was, the more severe the initial threshold shift.

Ryals et al. (1995), Salvi et al. (1998), and Cotanche (1999) have shown that structures such as the tegmentum vasculosum, which provides the endolymphatic potential in birds, the tectorial membrane, and neural synapses may also be damaged immediately after acoustic trauma. There are two important conclusions from these studies. One is that even when exposure and test conditions are identical, the amount of damage and the time course of loss and recovery from acoustic trauma are quite different among species. The second conclusion is that determination of the direct role of regenerated hair cells in the recovery of hearing after acoustic overstimulation is confounded by the continuing presence of nonregenerated hair cells on the papilla after initial acoustic trauma, the initial and continuing damage to other structures within the inner ear such as the tectorial membrane, and the fact that a considerable amount of hearing can return before a full complement of hair cells is replaced through regeneration.

These behavioral results are paralleled by a wealth of physiological data. Measures of CAP and evoked potential (EP) thresholds, for instance, have also shown a recovery from acoustic trauma in birds. In pigeons, CAP thresholds increased immediately after exposure to a 0.7-kHz tone at 136–142 dB SPL for 1 hour, but showed some recovery in most subjects (Müller et al. 1996, 1997). The time course of recovery varied somewhat among individual subjects, and some animals showed no recovery. A residual threshold shift of 26.3 dB remained at 2.0 kHz for some of the animals that recovered, while others showed normal thresholds within 3 weeks after exposure. Newborn chicks and adult chickens also show increased CAP and EP thresholds immediately after acoustic trauma, but animals with longer survival times showed near-normal thresholds (McFadden and Saunders 1989; Adler et al. 1992, 1993; Pugliano et al. 1993). Interestingly, less recovery occurred when chicks were exposed a second time (Adler et al. 1993).

Threshold shifts to a pure tone overexposure (Fig. 4.1A) and to narrowband noise overexposure (Fig. 4.1B) are shown across several species of birds. Although the exposure durations, intensities, and frequencies differed across species, these recovery curves represent virtually all of the existing data available on experiments that tested the same subjects repeatedly. Given the large differences in susceptibility to acoustic trauma both within and across species, these types of experiments are important for understanding the nature of the time course of recovery in individual subjects. These figures highlight the similarities in recovery times across species, even when the extent of the initial hearing loss is quite different.