The role of cholinergic transmission in outer hair cell functioning evaluated by distortion product otoacoustic emissions in myasthenic patients

Outer hair cells (OHCs) are the source of otoacoustic emissions, following a tropomyosin-miosin-dependent contraction, which are regulated by the oliv ocochlear bundle via the release of acetylcholine (ACh). ACh acts on ACh re ceptors (AChR) located on the OHC post-synaptic membrane. In myasthenia gra vis (M.G.) neuromuscular transmission is reduced due to the action of AChR autoantibodies. It has previously been shown that M.G. induces a reduction in transient evoked otoacoustic emissions (TEOAEs), which is reversed after administration of a cholinesterase (AChE) inhibitor. Distortion product ot oacoustic emissions (DPOAEs) were recorded before and 60 min after oral adm inistration of 60 mg pyridostigmine bromide in 25 patients with normal hear ing affected by M.G. The results were compared with those from 25 age-match ed normal controls. Mean values of DPOAE amplitude in myasthenic patients w ere significantly (p < 0.05) lower at all frequencies before drug administr ation. All patients showed an overall significant (p < 0.05) increase in DP OAE amplitude after drug administration, although without reaching the cont rol values. Such a recovery was more evident and highly significant (p < 0. 01) for middle and high frequencies and could be explained by a higher conc entration of ACh receptors in the basal and middle cochlear turns. These da ta seem to confirm the role of ACh in the neurotransmission of the auditory efferent system and may represent a new in vivo model for the investigatio n of the physiology of this system.