Chemical neuroprotection in the cochlea: The modulation of dopamine release from lateral olivocochlear efferents

Disruption of lateral olivocochlear neurons with a dopaminergic neurotoxin depresses spontaneous auditory nerve activity

“…New data from Liberman, et al [24] clearly show the results of selective LOC lesions on sound-evoked AN activity increase with age in mice, thus long-term post-lesion survival may have an important effect on outcomes. Perhaps even more important, however, MPTP lesions are limited to the subpopulation of LOC fibers that contain DA [for discussion and reviews, see 1, 7, 12, 18, 34]. The most parsimonious interpretation of the current data is that the observed shift in AN spontaneous activity after LOC disruption was produced by disrupting an otherwise tonic release of excitatory transmitter substances from a subset of the LOC terminals.…”

“…In addition, a small number of LOC neurons synapse directly on IHCs [21, 40, 41]. LOC efferents contain a variety of neurotransmitters, including dopamine (DA), dynorphin (dyn), enkepalin (enk), γ-aminobutyric acid (GABA), acetylcholine (ACh), and calcitonin-gene-related peptide (CGRP) [for reviews, see 1, 7, 12, 16, 18, 34]. There is significant transmitter co-localization, although the pattern varies across reports [4, 26, 36-38].…”

Regulation of dopamine D2 receptors in the guinea pig cochlea

“…Alternatively, a DA transporter has been discovered in the vicinity of Deiter's cells underneath OHCs [14]. Furthermore, DA released by lateral efferents might diffuse to OHCs and act in a paracrine fashion, as has been suggested for urocortin [15].…”

An investigation of hearing impairment in de-novo Parkinson's disease patients: A preliminary study

“…Notably, an excessive release of glutamate from IHC has been shown to induce an excitotoxic damage of primary auditory neurons [4]. Dopamine, which is released from lateral olivocochlear (LOC) efferent fibers below IHC, plays a significant modulating function on afferent dendrites, thus counteracting glutamate-excitotoxic effects [5]. Recent evidence of a possible otoprotective role of rasagiline, a MAO inhibitor commonly prescribed in PD, acting as a dopaminergic neurotransmission enhancer, provided support for this neuroprotective mechanism [6].…”