ANÁLISIS DE LA COMUNICACIÓN PRODUCIDA POR Y DESDE LAS ASOCIACIONES VALLISOLETANAS DE

The mechanical events in the cochlea are transduced into alterations of electrical potentials and ultimately into neural activity.

The endolymphatic space has a standing (resting) potential of about +80 mV with

respect to the perilymphatic space, which is related to the unequal distribution of Na+ and K+ between the endolymph and perilymph (about 140 mmol/1 K+ and 3 mmol/1 Na+ in endolymph and 4 mmol/1 K+ and 140 mmol/1 Na+ in the perilymph), and is maintained by active transport processes in the stria vascularis. Since at rest, the IHC and OHC have a

cell potential (membrane potential) of -70 mV and -40 mV, respectively, there is a potential difference of 150 mV and 120 mV, respectively, across ciliated cell membrane (cell interior negative). Additionally, the K+ concentration of about 140 mmol/1 in the endolymph is roughly the same as in the hair cells, so that the K+ equilibrium potential (NB. corresponds to equilibrium concentration - when electrochemical gradient of K+ is zero) amounts to 0 mV. Thus, the entire 150 mV and 120 mV, respectively, are available as driving forces for a K+ influx.

When sound-driven propagating travelling waves induce ciliar shearing that opens mechanosensitive K+ channels, then there is an influx of Ca ++ and K+ and the cell is

depolarised, providing a receptor potential which causes the release of neurotransmitter

(see below in the section 1.2.7). The displacement of stereocilia in the opposite direction, reduces K+ influx, the cells become hyperpolarised and less transmitter is released. The

receptor potential subsequently initiates the action potential in the corresponding

afferent fibres of the auditory nerve.

In the OHCs, the passive vibrations and sound-induced ionic gating leading to

depolarisation, is accompanied by the additional induction of active mechanical movement in the OHC cytoskeleton. Thus, sound-driven mechanical movements induce depolarisation of the electrical potential and a raised intracellular CaT+ induces fast a.c. contractions, shortening, of OHCs. The subsequent hyperpolarisation leads to slow d.c. movements, lengthening of OHC (Zenner, 1986), thus creating highly nonlinear and saturating positive feedback system. The OHC a.c. motility, which enhances the basilar membrane motion (near hearing threshold amplification by « 40 dB), is linearly correlated to the intensity of sound stimuli (LePage, 1987). However, with an increase in sound pressure level, the cochlea is capable of correcting undesirable (high) shifts of the basilar membrane by the OHC d.c. movements, leading to reduction of the passive displacement, and nonlinear compression of cochlear dynamics (attenuation). Thus, OHC act as controlled mechano-amplifiers within the cochlea and feed amplified mechanical oscillations to the IHCs, which are directly involved in the transformation of mechanical energy into neural activity.

There are three groups of gross stimulus-evoked potentials that can be recorded when electrodes are placed near the cochlea.

i.) Microphone potential or cochlear microphonic is an a.c. phenomenon. It reflects, like a microphone, the temporal course of the sound stimulus as fluctuation in voltage, thought to derive from OHC activity.

ii.) Summation potential, is a d.c. shift in the baseline potential, resulting from the

activity both, of IHCs and OHCs.

iii.) Compound action potential is the massed, synchronised activity of the auditory

1.2.4 Innervation of the cochlea

The organ o f Corti has afferent and efferent innervation (Figure 1.3). Afferent fibres that arborize around the bases o f the hair cells are dendrites from bipolar cells whose bodies are located in the spiral ganglion within the modiolus, the bony core around which the cochlea is wound. Efferent fibres are axonal endings o f neurons located in the brain stem. About 90-95% (Spoendlin,1979) o f 30,000 type I afferents (thin, unmyelinated) originate from the IHC (about 10-20 unbranched fibres are attached to each IHC), while approximately 5-10% o f the type II afferents (large, myelinated) originate from the OHCs (one fibre serves about 10 OHCs). This means that, although the OHCs by far outnumber the IHCs, the information transferred from the cochlea almost exclusively comes from the IHCs.

ORGAN O F CORTI N e u ro n T y p e ) G a n g lio n Ceti N e u ro n Wooiai C C i :■ A fferent , - . E fferent S u p erio r O livary C o m p le x T y p e li G a nglion Cell in n e r H air Cell O u te r H air C eils C o c h le a r N erve

Figure 1.3: The afferent and efferent innervation o f the cochlea (Schuknecht HF. Pathology o f the ear. Philadelphia: Lea & Febiger, 1993: p. 67)

In contrast, about 95% of all 1800 efferent fibres have direct and wide synaptic contact with the OHC bodies, whilst an almost negligible number of the efferent neurons have indirect postsynaptic contact with IHCs, via the dendrites of the afferent neurons innervating IHCs. The afferent fibres, forming the cochlear nerve, and efferent fibres, forming the olivo-cochlear bundle and travelling along the vestibular nerve, leave the cochlea, pass together through the internal auditory meatus and enter the brainstem at the upper part of medulla oblongata, at the level of the prepontine fossa.

This distinctly different innervation pattern implies specific physiological roles of the dual sensory system (IHCs and OHC)s in the cochlea: IHCs as the primary sensory cells that generate action potentials in the auditory nerve and OHCs as the active mechanoreceptors.

The cochlea also receives sympathetic, adrenergic innervation through the fibres ending on blood vessels in the spiral lamina and fibres terminating near afferent fibres

(Spoendlin and Lichtensteiger, 1966; Brechtelsbauer et al., 1990), as well as perivascular fibres in the stria vascularis (Liu et al., 1996). The presence of adrenergic innervation in the cochlea implies its role in controlling vasomotor tone and the influence on cochlear hemodynamics.