Table 3.

Studies of MOC protection, describing noise exposure conditions and effects of de-efferentation

Studies of MOC protection, describing noise exposure conditions and effects of de-efferentation
Authors	Species	Exposure details	Results	Conclusions of study
Cody and Johnstone (1982)	Guinea pig	10.0 kHz sinusoid, 107 dB SPL for 1 min	TTS to ipsilateral exposure was reduced with contralateral stimulation or contralateral cochlear destruction.	Acoustic activation of the efferent syste might be responsible for reduced threshold shifts.
Handrock and Zeisberg (1982)	Guinea pig	4-kHz octave-band noise, 120 dB SPL for 5 min or 125 dB SPL for 30 min	For 120 dB SPL exposure, there was no effect of de-efferentation on PTS; for 125 dB SPL exposure, de-efferentation resulted in significantly greater PTS after 8 days compared with normal animals.	Results suggest MOC might offer PTS protection from high-SPL, long-duration noise exposures.
Rajan and Johnstone (1983)	Guinea pig	10.0 kHz sinusoid, 97 or 103 dB SPL for 1 min	TTS to monaural exposure was reduced when contralateral stimulation, matched in frequency, was concurrent with exposure. The effect was lost when strychnine was given to block MOC.	MOC action can provide protection from intense noise exposure to cochlea.
Rajan (1988a)	Guinea pig	10.0 kHz sinusoid, 103 dB SPL for 1 min	TTS was reduced with electrical stimulation of COCB at IVth ventricle; protection was blocked by strychnine. COCB protection persisted after cessation of electrical stimulation. Effects were blocked by COCB lesion	COCB action might protect cochlea from intense monaural tone exposure TTS. Persistence of COCB protection is not accomplished in cochlea, but centrally.
Rajan (1988b)	Guinea pig	10.0 kHz sinusoid, 97, 101, 103, or 106 dB SPL for 1 min	TTS at 14 kHz was reduced for highest-level monaural exposure tones in presence of COCB stimulation at IVth ventricle. COCB protection is greater at the highest electrical pulse rates.	COCB protection is graded in effectiveness. Level of MOC protection increases with exposure conditions that produce the largest TTS.
Rajan and Johnstone (1988a)	Guinea pig	10.0 kHz sinusoid, 103 dB SPL for 1 min	TTS was reduced with electrical stimulation of COCB at round window; protection was blocked by strychnine. COCB protection persisted after cessation of electrical stimulation. Effects were blocked by COCB lesion.	COCB acts to protect cochlea from monaural acoustic trauma; COCB protection persists for up to 7 min poststimulation for 1 min COCB stimulation period. Persistent effects are not due to cochlear effects but result from “resetting” of some entral site.
Rajan and Johnstone (1988b)	Guinea pig	10 kHz sinusoid, 97, 101, 103, or 106 dB SPL for 10 s to 30 min	TTS was reduced with electrical stimulation of COCB at round window; protection was blocked by strychnine. The greater the potential damage of exposure, the greater the COCB protection; increases in COCB stimulation rate increased protection at mid- and high TTS exposures.	COCB acts to protect cochlea against TTS. Protection level is graded, increases with TTS level, increases with COCB stimulation rate/level.
Rajan and Johnstone (1988c)	Guinea pig	10 kHz sinusoid, 97, 101, 103, 106, or 110 dB SPL for 30 s or 1 min	TTS reduced with low-level contralateral acoustic stimulation; protection blocked by OCB lesion. The greater the potential damage of exposure, the greater the protection; increases in acoustic stimulation level increased protection at mid- and high TTS exposures. Protection was evident only with TTS level over 25 dB. Contralateral-induced protection persists.	COCB stimulated by contralateral sound acts to protect cochlea against TTS in a manner similar to that seen with electrical stimulation of COCB at IVth ventricle or round window. Protection persists for 5–7 min by activation of “central” site, which antidromically stimulates cochlea, rather than persistence acting in cochlea.
Hildesheimer et al. (1990)	Guinea pig	4.0 kHz sinusoid, 120 dB SPL for 20 min	De-efferentation or destruction of contralateral cochlea resulted in statistically less TTS. De-efferentation alone did not affect TTS. Destruction of contralateral ear resulted in greater TTS in de-efferented ear.	Data suggest no consistent efferent protection. Authors suggest inconsistencies with other studies showing protection may be due to specifics of experimental/stimulus conditions.
Liberman (1991)	Cat	6.0 kHz sinusoid, 100 dB SPL for 10 min. Exposure tone intensities were balanced in the two ears (intensity-balanced binaural exposures)	Within subjects, no differences were seen in comparisons of the PTS in normal and de-efferented ears. There was no protective effect of direct electrical stimulation of the efferents on floor of IVth ventricle.	In contrast with guinea pig studies, these studies suggest efferents are not involved in protecting the ear from noise trauma and suggests that differences in findings in other studies may be due to species differences, contribution of middle ear muscles, and/or cochlear blood flow changes.
Patuzzi and Thompson (1991)	Guinea pig	10.0 kHz sinusoid, 115 dB SPL for 60 or 150 s	TTS in CM and CAP measures was reduced in presence of low-level contralateral acoustic stimulation. This effect was lost when the MOC is sectioned. Interanimal variability in TTS was reduced following MOC lesions.	MOCs offer protection from acoustic trauma. Reductions in interanimal variability suggests MOCs have varying tonic effects on normal cochlear function across subjects.
Takeyama et al. (1992)	Guinea pig	2.0 kHz sinusoid, 110–130 dB SPL for 3–30 min	With electrical stimulation of COCB, TTS was reduced. Reduction in TTS, however, was evident only with TTS of >50–55 dB; with TTS <50 dB, there was no benefit of COCB stimulation.	Electrical stimulation of COCB can elicit protective mechanism for high-level acoustic trauma.
Liberman and Gao (1995)	Guinea pig	Narrowband noise (500 Hz bandwidth, centered at 10.0 kHz), 109 or 112 dB SPL for 2 h	109 dB SPL: No statistical differences in PTS or hair cell/stereocilia damage between normal and de-efferented ears. 112 dB SPL: Small statistical PTS difference, but no histologic differences between normal and de-efferented ears.	For conditions tested, there was no significant protective effect of MOC on CAP PTS or resulting hair cell damage for these relatively long-duration exposures. Given site of damage to the 112 dB SPL, they suggest the PTS protection observed is due to “slow” efferent effect.
Rajan (1995a)	Cat	3.0, 7.0, or 11.0 kHz sinusoids at 100 dB SPL for 10 min	Unilateral COCB cuts produced greatest TTS in the de-efferented ear for 11.0 kHz binaural exposures but not for 3.0 kHz or monaural exposures. MEMs had no effect on TTS.	OCB protection effects comparable in cats and guinea pigs. MOC protection might be frequency dependent.
Rajan (1995b)	Cat	3.0, 5.0, 7.0, 11.0, 15.0, 20.0 kHz sinusoids at 100–106 dB SPL for 7 to 40 min	The magnitude of the TTS was frequency and intensity dependent and required binaural exposure. The magnitude of protection increased with exposure intensity.	The magnitude of OCB protection to binaural exposures are frequency and intensity dependent. Across frequencies, protection was comparable for different exposure intensities that would produce comparable damage.
Reiter and Liberman (1995)	Guinea pig	6.0, 8.0, and 10.0 kHz sinusoids at 104–118 dB SPL for 1–5 min	OC is activated by electrical stimulation at IVth ventricle. Protection evident at 8.0 and 10.0 kHz for 1–2 min exposures. Protective effect is lost when OC stimulation preceded exposure.	Circumstantial evidence that protection occurs at 8.0 kHz and above, where “slow” efferent effects are observed, and not at 6.0 kHz, where “fast” OC effects are apparent, suggests protection is based on “slow” OC response.
Rajan (1996)	Cat	11.0 kHz sinusoid at 10 dB SPL for 10 min	Magnitude of OCB-mediated protection was unchanged over extended recording intervals (~30 h).	Because OCB-mediated protection did not change over time, but COCB contralateral suppression effects have been shown in some studies to change with time, OCB protection is mediated by a different efferent subgroup.
Zheng et al. (1997)	Chinchilla	105 dB SPL, broadband noise, for 6 h. Noise band “shaped” to produce “flat” hearing loss	Following noise exposure, de-efferented ears showed significant depression of DPOAE amplitudes and I/O functions compared with control and sham ears. There were no significant differences in CM amplitudes, I/O functions, or OHC loss following acoustic trauma between control and de-efferented ears.	Authors suggest data indicate that de-efferentation increases susceptibility to acoustic trauma. With de-efferentation, susceptibility to noise trauma is evident at low as well as high frequencies.
Rajan (2000)	Cat	13.0 kHz sinusoid at 100 dB SPL for 15 min	In the absence of efferents, moderate noise increases acoustic trauma to exposure tone. In normal ear, added noise increases efferent protection.	Author suggests added moderate noise activates efferents that are not otherwise stimulated by 100 dB SPL binaural tones, thus increasing efferent protection. In a de-efferented ear, the otherwise harmless noise exacerbates the TTS caused by the tonal exposure.
Zheng et al. (2000)	Chinchilla	150 dB pSPL, 100 impulses, 50 s total duration	No difference in TTS or loss of OHCs between control and de-efferented ears. De-efferentation resulted in a significantly greater PTS and loss of IHCs.	OHC susceptibility to acoustic trauma unaffected by de-efferentation. Significant increase in PTS and greater loss of IHCs following de-efferentation suggests MOC might play a role in protecting ear from noise trauma. It is unclear, however, why de-efferentation affects IHCs and not OHCs.
Rajan (2001a)	Cat	11 kHz sinusoid at 100 dB SPL for 10 min	Ipsilateral TTS is reduced in the unilaterally exposed (normal) ear when there is a partial unilateral hearing loss in the contralateral ear, due to “chronic resetting of noise susceptibility.” In cases of partial unilateral hearing loss, binaural exposure exacerbates the TTS. With total unilateral hearing loss, TTS in the normal ear was reduced.	The effects of intense sound exposure are different in bilaterally normal ears and in conditions of unilateral hearing loss. They also suggest CMOCs and UMOCS may exert different effects at the OHCs.
Rajan (2001c)	Cat	Narrowband noise 1.0–6.0 kHz (40 min) or 8.0–13.0 kHz (15 min) at 100 dB SPL	For both noise bands, the crossed-MOC offered small protection against noise trauma at frequencies within the exposure noise band. At frequencies above the noise band, it exacerbated the TTS. The uncrossed MOC showed no protective effects within the 1.0–6.0 kHz noise band, but showed a small protection for the frequencies within the 8–13.0 kHz noise band. The uncrossed MOC protected against the crossed-MOC-induced-high-side frequency increased susceptibility.	The crossed and uncrossed MOC subsystems interact in complex ways to affect the susceptibility of the cochlea to noise trauma and may form the basis for a contrast-enhancement mechanism to increase the detection of tones in noise.