Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nerve-fiber regeneration in the chinchilla cochlea following a traumatic noise exposure was systematically described by Bohne and Harding (1992). However, their study did not determine the origin of the regenerated nerve fibers (RNFs). In the present study, 23 chinchillas were exposed for 12 h to a 0.5 kHz octave band of noise at 120 dB SPL. After a 3-month or 1-year recovery period, their right cochleas were incubated to demonstrate acetylcholinesterase (AChE) activity and then briefly counterstained with Neutral Red or OsO4. Their left cochleas were fixed with OsO4 and dissected using a combined organ of Corti (OC)/modiolus technique that preserved both structures for high-resolution microscopy. All cochleas were prepared as plastic-embedded flat preparations. Damage was located in the basal two-thirds of the cochlea and generally consisted of multiple lesions in the OC, often involving total degeneration of one or more OC segments (i.e., OC wipeouts). The OC wipeouts were separated from one another by areas which contained some identifiable cells of the OC (i.e., OC remnants). Most RNFs were found in OC wipeouts adjacent to OC remnants. In those animals (83%) with significant OC damage, 13 (100%) 3-month-recovery chinchillas had 1-96 RNFs while 6 (86%) 1-year-recovery chinchillas had 7-62 RNFs. In the AChE-stained cochleas, none of the RNFs were AChE-positive, but normal AChE-positive fibers were found in the undamaged apical turn. A variable number of surviving spiral ganglion cells was present in those regions of Rosenthal's canal that had originally innervated the missing hair cells in the OC wipeouts and remnants. It is concluded that RNFs are not part of the efferent cochlear system and therefore, most likely belong to the afferent system.
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PMID:Regenerated nerve fibers in the noise-damaged chinchilla cochlea are not efferent. 864 46

Previous work has shown that the cochlear efferent system may play a role in protecting the ear from noise-induced temporary threshold shifts (TTS) following exposures to a single tone or series of moderate-level noises ('toughening'). However, whether the olivocochlear bundle (OCB) is important in decreasing noise-induced permanent threshold shifts (PTS) remains an open question. The importance of the OCB in decreasing the ear's susceptibility to noise, as reflected by 2f1-f2 distortion product otoacoustic emissions, was assessed by sectioning both the ipsilateral and contralateral divisions of the efferent system and exposing chinchillas while awake to an octave band noise (4 kHz) at a low level (85 dB SPL) for 10 days (6 h/day) and then at a high level (95 dB SPL) for 48 h. Complete de-efferentation was verified by cochlear acetylcholinesterase staining. The ears that were de-efferent showed substantially more TTS, greater PTS and larger cochlear lesions of outer hair cells. The results suggest that the efferent system may influence the ear's ability to develop resistance to noise trauma.
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PMID:The role of the cochlear efferent system in acquired resistance to noise-induced hearing loss. 911 63

The effects of impulse noise (firecrackers at 170 dB SPL, 1, 10, 20 rounds) on auditory cortical response threshold (CRT) and activity of succinic dehydrogenase (SDH) and acetylcholinesterase (AchE) in the inner ear were studied in 37 guinea pigs. The results showed that extent of damage in the cochlea was related to amount of exposure to the noise. Exposure to 10 rounds resulted in temporal threshold shift (TTS); to 20 rounds the result was permanent threshold shift (PTS). For the period when TTS existed, inverse correlation was noticed between enzyme activity change and CRT shift. The correlation could not be established when PTS was induced. The results suggest that the pathomechanism of PTS was more complex than that of TTS. The significance of the results is discussed.
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PMID:Effects of impulse noise on cortical response threshold and inner ear activity of succinic dehydrogenase and acetylcholinesterase in guinea pigs. 987 Jun 25

A number of studies have shown that the ear can be protected from sound over-exposure, either by activating the cochlear efferent system, or by sound 'conditioning' in which the role of the efferent system is less certain. To study more definitively the molecular basis of deliberately induced cochlear protection from excessive sounds, it is advantageous to determine, for an inbred mouse strain, a range of noise exposure parameters that effectively alter cochlear function. As an initial step towards this goal, young CBA/CaJ mice were exposed to a 105-dB SPL octave-band noise (OBN), centered at 10 kHz, for various lengths of time consisting of 10 min, or 0.5, 1, 3, or 6 h. Distortion product otoacoustic emissions (DPOAEs) at the 2f1-f2 frequency, in response to equilevel primary tones of low to moderate levels, were used to quantify the damaging effects of these sound over-exposures on cochlear function. In addition, staining for acetylcholinesterase (AChE) activity to assess for noise-induced changes in the pattern of efferent-nerve innervation to the cochlea was also performed in a subset of mice that were exposed to the longest-lasting 6-h OBN. The 10-min OBN resulted in only temporary reductions in DPOAE levels, which recovered to pre-exposure values within 5 days. Increasing the exposure to 0.5 h resulted in permanent DPOAE losses that, for low primary-tone levels, were still present at 31 days post-exposure. Additionally, the 1-h and longer exposures caused permanent reductions in DPOAEs for all test levels, which were measurable at 31 days following exposure. Light-microscopic observations restricted to the 11-18-kHz frequency region of the organ of Corti, for a subset of mice exposed to the 6-h OBN, uncovered a significant loss of outer hair cells (OHCs). However, despite the OHC loss in this region, the AChE activity associated with the related pattern of efferent innervation remained largely intact.
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PMID:Temporary and permanent noise-induced changes in distortion product otoacoustic emissions in CBA/CaJ mice. 1137 80