PubMed1992
Direct observations of the basilar membrane movements show that sound perception can no longer be regarded as a passive process: vulnerable, energy-consuming amplification processes are required in the cochlea. The outer hair cells (OHC) fulfil this demand morphologically and functionally. These sensory cells have a double role: they perceive sound and thus modulate the cochlear biomechanics through their motile activity. The key event of sound transduction is performed by the inner hair cells (IHC) after active sound amplification in the OHC. The control of the OHC is assured by the efferent olivocochlear fibres which release acetylcholine (ACh) and gamma-aminobutyric acid (GABA) into the synaptic cleft at the basal pole of the OHC. Nicotinergic acetylcholine and GABA receptors within the outer cell membrane of OHC were identified and characterised. The application of the neurotransmitter GABA to the basal pole of vital OHC leads to a reversible elongation of the cylindrical cell body while ACh induces a reversible, slow contraction of the sensory cells. These two neurotransmitters are supposed to counteract in the control of the cochlear amplifier. The reciprocal distribution of ACh and GABA receptors and their counteracting function (contraction vs elongation) has an additional impact on the modulation of OHC function. The result is an even more diversified control of the cochlear amplifier. The energy-consuming cochlear amplifications are reflected by an epiphenomenon, i.e. the otoacoustic emissions (OAE). These are emitted by the cochlea and can be divided into "spontaneous OAE", "transitory evoked OAE" (TEOAE), "stimulus frequency OAE" and "distortion product OAE". The TEOAE are now an integrated part of audiological diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)