Structure of the Mammalian Cochlea

Purinergic signaling has broad physiological significance to the hearing organ, involving signal transduction via ionotropic P2X receptors and metabotropic G-protein-coupled P2Y and P1 (adenosine), alongside conversion of nucleotides and nucleosides by ectonucleotidases and ecto-nucleoside diphosphokinase. In addition, ATP release is modulated by acoustic overstimulation or stress and involves feedback regulation. Many of these principal elements of the purinergic signaling complex have been well characterized in the cochlea, while the characterization of P2Y receptor expression is emerging. The present study used immunohistochemistry to evaluate the expression of five P2Y receptors, P2Y 1 , P2Y 2 , P2Y 4 , P2Y 6 , and P2Y 12 , during development of the rat cochlea. Commencing in the late embryonic period, the P2Y receptors studied were found in the cells lining the cochlear partition, associated with establishment of the electrochemical environment which provides the driving force for sound transduction. In addition, early postnatal P2Y 2 and P2Y 4 protein expression in the greater epithelial ridge, part of the developing hearing organ, supports the view that initiation and regulation of spontaneous activity in the hair cells prior to hearing onset is mediated by purinergic signaling. Sub-cellular compartmentalization of P2Y receptor expression in sensory hair cells, and diversity of receptor expression in the spiral ganglion neurons and their satellite cells, indicates roles for P2Y receptormediated Ca 2+ -signaling in sound transduction and auditory neuron excitability. Overall, the dynamics of P2Y receptor expression during development of the cochlea complement the other elements of the purinergic signaling complex and reinforce the significance of extracellular nucleotide and nucleoside signaling to hearing.

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“…5i,j). The type II fibrocytes [33] at the insertion point of Reissner's membrane showed strong P2Y 2 expression at P6 (Fig. 3b).…”

Section: P2y Receptor Expression Around the Onset Of Hearing (P6-p12)mentioning

confidence: 93%

Differential expression of P2Y receptors in the rat cochlea during development

Huang

Thorne

Vlajkovic

et al. 2010

Purinergic Signalling

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“…Fibrocytes of the spiral ligament are divided into four cell types Schulte 1991, 1996;Slepecky 1996) based on histologic characteristics, immunostaining patterns, and general location (Fig. 4).…”

Section: Figmentioning

confidence: 99%

Lateral Wall Histopathology and Endocochlear Potential in the Noise-Damaged Mouse Cochlea

Hirose

Liberman

2003

JARO - Journal of the Association for Research in Otolaryngolog

249

221

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Noise exposure damages the stria and spiral ligament and may contribute to noise-induced threshold shift by altering the endocochlear potential (EP). The aim of this study was to correlate lateral wall histopathology with changes in EP and ABR thresholds. CBA/CaJ mice were exposed to octave band (8-16 kHz) noise for 2 h at intensities ranging from 94 to 116 dB SPL and evaluated 0 h to 8 weeks postexposure. EP in control mice averaged 86 and 101 mV in apical and basal turns, respectively. The 94 dB exposures caused a 40 dB temporary threshold shift (TTS), and there was with no corresponding change in EP. The 112 and 116 dB exposures caused >60 dB threshold shifts at 24 h, and EP was transiently decreased, e.g., to 21 and 27 mV in apical and basal turns after 116 dB. By 1 week postexposure, EP returned to control values in all exposure groups, although those exposed to 112 or 116 dB showed large permanent threshold shifts (PTS). Cochleas were plastic-embedded and serialsectioned for light microscopic and ultrastructural analysis. Acute changes included degeneration of type II fibrocytes of the spiral ligament and strial edema. The strial swelling peaked at 24 h when significant EP recovery had taken place, suggesting that these changes reflect compensatory volume changes. In the chronic state, massive loss of type II fibrocytes and degeneration of strial intermediate and marginal cells was observed with drastic reduction in membrane surface area. The results suggest that EP shifts do not occur with TTS and also do not add significantly to PTS in the steady state. However, EP loss could contribute to acute threshold shifts that resolve to a PTS. EP recovery despite significant strial degeneration may be partly due to decreased transduction current caused by hair cell damage.

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“…In mammals, each of 5-30 AFs contacts one inner hair cell (IHC) through a single, unbranched dendrite (6). In this study, we took advantage of this unique innervation pattern to characterize directly the transfer function at a single IHC ribbon synapse.…”

mentioning

confidence: 99%

Time course and calcium dependence of transmitter release at a single ribbon synapse

Goutman

Glowatzki

2007

Proc. Natl. Acad. Sci. U.S.A.

221

322

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At the first synapse in the auditory pathway, the receptor potential of mechanosensory hair cells is converted into a firing pattern in auditory nerve fibers. For the accurate coding of timing and intensity of sound signals, transmitter release at this synapse must occur with the highest precision. To measure directly the transfer characteristics of the hair cell afferent synapse, we implemented simultaneous whole-cell recordings from mammalian inner hair cells (IHCs) and auditory nerve fiber terminals that typically receive input from a single ribbon synapse. During a 1-s IHC depolarization, the synaptic response depressed >90%, representing the main source for adaptation in the auditory nerve. Synaptic depression was slightly affected by ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor desensitization; however, it was mostly caused by reduced vesicular release. When the transfer function between transmitter release and Ca 2؉ influx was tested at constant open probability for Ca 2؉ channels (potentials >0 mV), a super linear relation was found. This relation is presumed to result from the cooperative binding of three to four Ca 2؉ ions at the Ca 2؉ sensor. However, in the physiological range for receptor potentials (؊50 to ؊30 mV), the relation between Ca 2؉ influx and afferent activity was linear, assuring minimal distortion in the coding of sound intensity. Changes in Ca 2؉ influx caused an increase in release probability, but not in the average size of multivesicular synaptic events. By varying Ca 2؉ buffering in the IHC, we further investigate how Ca 2؉ channel and Ca 2؉ sensor at this synapse might relate.hearing ͉ exocytosis ͉ hair cell ͉ synaptic transmission ͉ auditory nerve fiber M echanosensory hair cells of the inner ear release neurotransmitter continuously and with high temporal precision onto dendrites of auditory nerve fibers (AFs) (1); therefore, availability of releasable synaptic vesicles is critical. Synaptic ribbons, presynaptic structures presenting a halo of tethered vesicles, also found in retinal photoreceptors and bipolar cells (2), are thought to facilitate accumulation of vesicles presynaptically (3). Postsynaptically, ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors mediate fast synaptic transmission (4). The response of the cochlea to sound has been investigated in great detail: prolonged sound stimulation produces an increase in the firing activity of the auditory nerve that adapts on a milliseconds time scale (5). However, direct demonstration of the synaptic processes underlying adaptation and sustained release is still missing. Heretofore, hair cell exocytosis has been measured by changes in membrane capacitance that sum activity from all of the dozens of ribbon synapses in each cell (3). Capacitance measurements therefore cannot distinguish properties of individual ribbons and are limited in temporal resolution, requiring extrapolation for the earliest components. Nor does this approach reveal what role postsynaptic desensitization might play.I...

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Structure of the Mammalian Cochlea

Cited by 204 publications

References 265 publications

Differential expression of P2Y receptors in the rat cochlea during development

Differential expression of P2Y receptors in the rat cochlea during development

Lateral Wall Histopathology and Endocochlear Potential in the Noise-Damaged Mouse Cochlea

Time course and calcium dependence of transmitter release at a single ribbon synapse

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