[Serotonergic innervation of the auditory receptor]. / Inervación serotoninérgica del receptor auditivo.

The serotonergic inervation of the auditory receptor is composed by nerve fibres of multipolar neurons located on the superior lateral oliva. These neurons could correspond to outer elements of the nucleus reticularis caudalis. The peripheral projection on the auditory receptor is composed of varicose fibres distributed within the inner spiral bundle connecting on inner hair cells. Other fibres, after a spiral pathway within the Corti's tunnel, reach the outer hair cells. This new fascicle, with a particular origin and peripheral distribution, characterized as serotonergic and of unknown function, could be considered as a previously undescribed projection of the reticular formation on the auditory receptor.

Effects of acute and chronic administration of cyclosporine on dopamine metabolism in the rat cochlea.

The effect of cyclosporine (CyA) on dopamine (DA) metabolism at the cochlear level was analyzed. Adult male rats were submitted to CyA treatment at the doses of 1, 5 or 20 mg/Kg/day, for 1 day (acute) or 8 days (chronic). Cochlear contents of DA and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were measured by using high performance liquid chromatography (HPLC-ED). Either dose of acutely administered CyA did not modify cochlear DA content and markedly reduced that of DOPAC, in a non dose-dependent way. Acute administration of 5 mg/Kg of CyA decreased HVA content while the highest dose increased it. DOPAC/DA index was significantly reduced with either CyA dose, although HVA/DA index was not modified. Chronic treatment with CyA markedly reduced cochlear DA and DOPAC contents in a non dose-dependent way. However, HVA content decreased after the highest administration dose of the drug. DOPAC/DA index was further reduced after the drug chronic administration. An increased HVA/DA index was surprisingly observed, after chronic administration of either dose of the drug, the response being dose- dependent. These data show that acute treatment with CyA mainly affects the DA reuptake, while chronic treatment affected both DA reuptake and metabolism at the cochlear level.

Neurotransmitters of the olivocochlear lateral efferent system: with an emphasis on dopamine.

The olivocochlear lateral efferent system (OLES) of the adult mammalian cochlea uses variety of neuroactive substances, such as acetyl choline, GABA, dopamine (DA), enkephalins, dynorphins and CGRP. These neuroactive substances have been located within the efferent, small and dense matrix, fibers and terminals of the inner spiral and tunnel bundles. However, some of these neuroactive substances have also been found outside the OLES. Acetyl choline and CGRP, for instance, appear within the olivocochlear medial efferent fibers, and DA and CGRP may also be present in the perivascular innervation. A special case is GABA innervation at the apical coil, where nerve fibers containing GABA also make synapses with OHCs bodies. All these substances of the OLES could be involved in a highly selective filter modulating the activity of primary afferent fibers. For instance, sound stimulation results in an increase of cochlear DA turnover, indicating the release of DA from OLES fibers. DA probably acts on D-2 receptors since the administration of piribedil, a D-2 agonist, results in blocking of noise effects, while D-1 receptor stimulation does not modify cochlear DA turnover induced by noise. Therefore, DA could play an important role in the modulation and noise-protection of cochlear primary afferents. During cochlear development, all the aforementioned neuroactive substances appear a long time before the onset of hearing (evidenced by the recording of cochlear compound action potential and microphonic potentials). Thus, they may act during development on the late reorganization and plasticity on the afferent and efferent fibers. Moreover, the positive neurotrophic effect observed in cultured cochlear neurons, with GABA or glutamate, add new support to that hypothesis.