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Journal articles on the topic 'Cochlea – Innervation'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Brown, M. Christian. "Single-unit labeling of medial olivocochlear neurons: the cochlear frequency map for efferent axons." Journal of Neurophysiology 111, no. 11 (June 1, 2014): 2177–86. http://dx.doi.org/10.1152/jn.00045.2014.

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Medial olivocochlear (MOC) neurons are efferent neurons that project axons from the brain to the cochlea. Their action on outer hair cells reduces the gain of the “cochlear amplifier,” which shifts the dynamic range of hearing and reduces the effects of noise masking. The MOC effects in one ear can be elicited by sound in that ipsilateral ear or by sound in the contralateral ear. To study how MOC neurons project onto the cochlea to mediate these effects, single-unit labeling in guinea pigs was used to study the mapping of MOC neurons for neurons responsive to ipsilateral sound vs. those responsive to contralateral sound. MOC neurons were sharply tuned to sound frequency with a well-defined characteristic frequency (CF). However, their labeled termination spans in the organ of Corti ranged from narrow to broad, innervating between 14 and 69 outer hair cells per axon in a “patchy” pattern. For units responsive to ipsilateral sound, the midpoint of innervation was mapped according to CF in a relationship generally similar to, but with more variability than, that of auditory-nerve fibers. Thus, based on CF mappings, most of the MOC terminations miss outer hair cells involved in the cochlear amplifier for their CF, which are located more basally. Compared with ipsilaterally responsive neurons, contralaterally responsive neurons had an apical offset in termination and a larger span of innervation (an average of 10.41% cochlear distance), suggesting that when contralateral sound activates the MOC reflex, the actions are different than those for ipsilateral sound.

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2

Brown, M. Christian. "Recording and labeling at a site along the cochlea shows alignment of medial olivocochlear and auditory nerve tonotopic mappings." Journal of Neurophysiology 115, no. 3 (March 1, 2016): 1644–53. http://dx.doi.org/10.1152/jn.00842.2015.

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Medial olivocochlear (MOC) neurons provide an efferent innervation to outer hair cells (OHCs) of the cochlea, but their tonotopic mapping is incompletely known. In the present study of anesthetized guinea pigs, the MOC mapping was investigated using in vivo, extracellular recording, and labeling at a site along the cochlear course of the axons. The MOC axons enter the cochlea at its base and spiral apically, successively turning out to innervate OHCs according to their characteristic frequencies (CFs). Recordings made at a site in the cochlear basal turn yielded a distribution of MOC CFs with an upper limit, or “edge,” due to usually absent higher-CF axons that presumably innervate more basal locations. The CFs at the edge, normalized across preparations, were equal to the CFs of the auditory nerve fibers (ANFs) at the recording sites (near 16 kHz). Corresponding anatomical data from extracellular injections showed spiraling MOC axons giving rise to an edge of labeling at the position of a narrow band of labeled ANFs. Overall, the edges of the MOC CFs and labeling, with their correspondences to ANFs, suggest similar tonotopic mappings of these efferent and afferent fibers, at least in the cochlear basal turn. They also suggest that MOC axons miss much of the position of the more basally located cochlear amplifier appropriate for their CF; instead, the MOC innervation may be optimized for protection from damage by acoustic overstimulation.

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3

Raphael, Yehoash, and Richard A. Altschuler. "Structure and innervation of the cochlea." Brain Research Bulletin 60, no. 5-6 (June 2003): 397–422. http://dx.doi.org/10.1016/s0361-9230(03)00047-9.

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4

Manley, Geoffrey A., and Christine Köppl. "Phylogenetic development of the cochlea and its innervation." Current Opinion in Neurobiology 8, no. 4 (August 1998): 468–74. http://dx.doi.org/10.1016/s0959-4388(98)80033-0.

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5

Lavigne-Rebillard, Mireille, and Rémy Pujol. "Hair Cell Innervation in the Fetal Human Cochlea." Acta Oto-Laryngologica 105, no. 5-6 (January 1988): 398–402. http://dx.doi.org/10.3109/00016488809119492.

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6

Bulankina, A. V., and T. Moser. "Neural Circuit Development in the Mammalian Cochlea." Physiology 27, no. 2 (April 2012): 100–112. http://dx.doi.org/10.1152/physiol.00036.2011.

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The organ of Corti, the sensory epithelium of the mammalian auditory system, uses afferent and efferent synapses for encoding auditory signals and top-down modulation of cochlear function. During development, the final precisely ordered sensorineural circuit is established following excessive formation of afferent and efferent synapses and subsequent refinement. Here, we review the development of innervation of the mouse organ of Corti and its regulation.

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7

Huang, Eric J., Wei Liu, Bernd Fritzsch, Lynne M. Bianchi, Louis F. Reichardt, and Mengqing Xiang. "Brn3a is a transcriptional regulator of soma size, target field innervation and axon pathfinding of inner ear sensory neurons." Development 128, no. 13 (July 1, 2001): 2421–32. http://dx.doi.org/10.1242/dev.128.13.2421.

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The POU domain transcription factors Brn3a, Brn3b and Brn3c are required for the proper development of sensory ganglia, retinal ganglion cells, and inner ear hair cells, respectively. We have investigated the roles of Brn3a in neuronal differentiation and target innervation in the facial-stato-acoustic ganglion. We show that absence of Brn3a results in a substantial reduction in neuronal size, abnormal neuronal migration and downregulation of gene expression, including that of the neurotrophin receptor TrkC, parvalbumin and Brn3b. Selective loss of TrkC neurons in the spiral ganglion of Brn3a−/− cochlea leads to an innervation defect similar to that of TrkC−/− mice. Most remarkably, our results uncover a novel role for Brn3a in regulating axon pathfinding and target field innervation by spiral and vestibular ganglion neurons. Loss of Brn3a results in severe retardation in development of the axon projections to the cochlea and the posterior vertical canal as early as E13.5. In addition, efferent axons that use the afferent fibers as a scaffold during pathfinding also show severe misrouting. Interestingly, despite the well-established roles of ephrins and EphB receptors in axon pathfinding, expression of these molecules does not appear to be affected in Brn3a−/− mice. Thus, Brn3a must control additional downstream genes that are required for axon pathfinding.

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8

Whitehead, M. C., and D. K. Morest. "The development of innervation patterns in the avian cochlea." Neuroscience 14, no. 1 (January 1985): 255–76. http://dx.doi.org/10.1016/0306-4522(85)90177-0.

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9

Wangemann, Philine, Hyoung-Mi Kim, Sara Billings, Kazuhiro Nakaya, Xiangming Li, Ruchira Singh, David S. Sharlin, Douglas Forrest, Daniel C. Marcus, and Peying Fong. "Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1435—F1447. http://dx.doi.org/10.1152/ajprenal.00011.2009.

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Mutations of SLC26A4 cause an enlarged vestibular aqueduct, nonsyndromic deafness, and deafness as part of Pendred syndrome. SLC26A4 encodes pendrin, an anion exchanger located in the cochlea, thyroid, and kidney. The goal of the present study was to determine whether developmental delays, possibly mediated by systemic or local hypothyroidism, contribute to the failure to develop hearing in mice lacking Slc26a4 ( Slc26a4−/−). We evaluated thyroid function by voltage and pH measurements, by array-assisted gene expression analysis, and by determination of plasma thyroxine levels. Cochlear development was evaluated for signs of hypothyroidism by microscopy, in situ hybridization, and quantitative RT-PCR. No differences in plasma thyroxine levels were found in Slc26a4−/− and sex-matched Slc26a4+/− littermates between postnatal day 5 ( P5) and P90. In adult Slc26a4−/− mice, the transepithelial potential and the pH of thyroid follicles were reduced. No differences in the expression of genes that participate in thyroid hormone synthesis or ion transport were observed at P15, when plasma thyroxine levels peaked. Scala media of the cochlea was 10-fold enlarged, bulging into and thereby displacing fibrocytes, which express Dio2 to generate a cochlear thyroid hormone peak at P7. Cochlear development, including tunnel opening, arrival of efferent innervation at outer hair cells, endochondral and intramembraneous ossification, and developmental changes in the expression of Dio2, Dio3, and Tectb were delayed by 1–4 days. These data suggest that pendrin functions as a HCO3− transporter in the thyroid, that Slc26a4−/− mice are systemically euthyroid, and that delays in cochlear development, possibly due to local hypothyroidism, lead to the failure to develop hearing.

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10

Gao, Jiangang, Stéphane F. Maison, Xudong Wu, Keiko Hirose, Sherri M. Jones, Ildar Bayazitov, Yong Tian, et al. "Orphan Glutamate Receptor δ1 Subunit Required for High-Frequency Hearing." Molecular and Cellular Biology 27, no. 12 (April 16, 2007): 4500–4512. http://dx.doi.org/10.1128/mcb.02051-06.

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ABSTRACT The function of the orphan glutamate receptor delta subunits (GluRδ1 and GluRδ2) remains unclear. GluRδ2 is expressed exclusively in the Purkinje cells of the cerebellum, and GluRδ1 is prominently expressed in inner ear hair cells and neurons of the hippocampus. We found that mice lacking the GluRδ1 protein displayed significant cochlear threshold shifts for frequencies of >16 kHz. These deficits correlated with a substantial loss of type IV spiral ligament fibrocytes and a significant reduction of endolymphatic potential in high-frequency cochlear regions. Vulnerability to acoustic injury was significantly enhanced; however, the efferent innervation of hair cells and the classic efferent inhibition of outer hair cells were unaffected. Hippocampal and vestibular morphology and function were normal. Our findings show that the orphan GluRδ1 plays an essential role in high-frequency hearing and ionic homeostasis in the basal cochlea, and the locus encoding GluRδ1 represents a candidate gene for congenital or acquired high-frequency hearing loss in humans.

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11

Ivanov, Emylian A., and Nikolai E. Lazarov. "Postnatal development of the afferent innervation of the mammalian cochlea." Biomedical Reviews 23 (December 31, 2012): 37. http://dx.doi.org/10.14748/bmr.v23.27.

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12

Vass, Z., S. E. Shore, A. L. Nuttall, G. Jancsó, P. B. Brechtelsbauer, and J. M. Miller. "Trigeminal ganglion innervation of the cochlea—a retrograde transport study." Neuroscience 79, no. 2 (May 1997): 605–15. http://dx.doi.org/10.1016/s0306-4522(96)00641-0.

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13

Robertson, Donald, Alan R. Harvey, and K. Stewart Cole. "Postnatal development of the efferent innervation of the rat cochlea." Developmental Brain Research 47, no. 2 (June 1989): 197–207. http://dx.doi.org/10.1016/0165-3806(89)90176-4.

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14

Usami, Shin-Ichi, Jiro Hozawa, Masayuki Tazawa, Toshio Yoshihara, Makoto Igarashi, and Glenn C. Thompson. "Immunocytochemical Study of Catecholaminergic Innervation in the Guinea Pig Cochlea." Acta Oto-Laryngologica 105, sup447 (January 1988): 36–45. http://dx.doi.org/10.3109/00016488809102855.

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15

Gunewardene, Niliksha, Duncan Crombie, Mirella Dottori, and Bryony A. Nayagam. "Innervation of Cochlear Hair Cells by Human Induced Pluripotent Stem Cell-Derived NeuronsIn Vitro." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1781202.

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Induced pluripotent stem cells (iPSCs) may serve as an autologous source of replacement neurons in the injured cochlea, if they can be successfully differentiated and reconnected with residual elements in the damaged auditory system. Here, we explored the potential of hiPSC-derived neurons to innervate early postnatal hair cells, using establishedin vitroassays. We compared two hiPSC lines against a well-characterized hESC line. After ten days’ coculturein vitro, hiPSC-derived neural processes contacted inner and outer hair cells in whole cochlear explant cultures. Neural processes from hiPSC-derived neurons also made contact with hair cells in denervated sensory epithelia explants and expressed synapsin at these points of contact. Interestingly, hiPSC-derived neurons cocultured with hair cells at an early stage of differentiation formed synapses with a higher number of hair cells, compared to hiPSC-derived neurons cocultured at a later stage of differentiation. Notable differences in the innervation potentials of the hiPSC-derived neurons were also observed and variations existed between the hiPSC lines in their innervation efficiencies. Collectively, these data illustrate the promise of hiPSCs for auditory neuron replacement and highlight the need to develop methods to mitigate variabilities observed amongst hiPSC lines, in order to achieve reliable clinical improvements for patients.

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16

Gil-Loyzaga, Pablo, M. Visitación Bartolomé, and M. Angeles Vicente-Torres. "Serotonergic innervation of the organ of corti of the cat cochlea." NeuroReport 8, no. 16 (November 1997): 3519–21. http://dx.doi.org/10.1097/00001756-199711100-00020.

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17

Raphael, Yehoash, Marc Lenoir, Romuald Wroblewski, and Remy Pujol. "The sensory epithelium and its innervation in the mole rat cochlea." Journal of Comparative Neurology 314, no. 2 (December 8, 1991): 367–82. http://dx.doi.org/10.1002/cne.903140211.

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18

Vass, Zoltán, Susan E. Shore, Alfred L. Nuttall, and Josef M. Miller. "Endolymphatic Hydrops Reduces Retrograde Labeling of Trigeminal Innervation to the Cochlea." Experimental Neurology 151, no. 2 (June 1998): 241–48. http://dx.doi.org/10.1006/exnr.1998.6813.

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19

Fermin, Cesar D. "Tritiated thymidine in the chick embryo inner ear." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 846–47. http://dx.doi.org/10.1017/s0424820100156213.

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Development of the chick (Gallus domesticus) inner ear has been studied, and the maturation of cells that detect sound has been analyzed at the E.M. level [1,2,3]. Other workers showed correspondence between ultrastructural maturation and behavioral responses [4,5]. In mammals [6] hair cells mature after ceasation of mitosis {Fig.l}, in a pattern so that older cells are in the base of the cochlea while younger cells are in the apex [7]. But, electrophysiology indicates that cells at the base do not function first. Chicks are precocious with well developed sensory organs at birth, and their embryonic development follows, on a very short time span, a sequence that resembles that of the human ear. This study was undertaken to standarize tritiated thymidine (TT) because resolution of TT in avian embryos differs significantly from mammals [6]. Embryos were injected with 100 μl of TT, and sacrificed 1 or 2 hours later in order to label only those cells that were actively dividing cells at the time of the injection. Specimens were fixed and processed for autoradiography [6].Actively dividing cells incorporate TT after short exposure, with minimal background. It seems that vestibular sensory epithelia {Fig.2} have more dividing cells than the auditory sensory epithelia {Fig.3}, even though the vestibule develop before the cochlea. The ratio between the number of labeled cells over the length of the sensory epithelia is lower in the auditory basilar papilla (0.098 cell/(μm) than in the vestibular utricle (0.77 cell/μm) and saccule (1.66 cell/ μm). When dividing cells were analyzed in the basilar papilla alone, and their distribution displayed along the length of the cochlea over time, older cells were opposite to the VIIIth nerve fibers that innervate those hair cells. A lateral and a longitudinal gradient has been established and hair cells closer to the nerve in the mid-basal area mature earlier than hair cells at both ends of the cochlea [2]. This finding, if occuring in mammals, may explain why mid-frequency are the first to appear [5]. The first 1/3 of the chick cochlea contains mainly short hair cells and are innervated primarily by efferent nerve fibers, which arrive in the cochlea almost a week after the afferent do. Moreover, tall hair cells extend 2/3 of the cochlear length from apex to mid-base and show mature innervation patterns before the short hair cells do. In the short embryonic cochlea, frequencies may be produced first in the what will later be the mid-region because, early in development, that area contains more mature receptors [1,2,3].

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20

Scheffel, Jennifer L., Samiha S. Mohammed, Chloe K. Borcean, Annie J. Parng, Hyun Ju Yoon, Darwin A. Gutierrez, and Wei-Ming Yu. "Spatiotemporal Analysis of Cochlear Nucleus Innervation by Spiral Ganglion Neurons that Serve Distinct Regions of the Cochlea." Neuroscience 446 (October 2020): 43–58. http://dx.doi.org/10.1016/j.neuroscience.2020.08.029.

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21

Husseman, Jacob W., Kwang Pak, Eduardo Chavez, and Allen Ryan. "R443 – Organotypic Co-Culture of Spiral Ganglion and Organ of Corti." Otolaryngology–Head and Neck Surgery 139, no. 2_suppl (August 2008): P192—P193. http://dx.doi.org/10.1016/j.otohns.2008.05.599.

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Problem The ability to carry out in vitro culture of the auditory neuroepithelium has provided a powerful means of studying inner ear development. Recently, we have developed an organotypic culture technique that mimics the perinatal cochlea in vivo. Methods Using sterile microdissection and in vitro methods, we have been able to co-culture explanted spiral ganglion (SG) with separate explanted organ of Corti (oC) from different neonatal mice. The SG and oC were co-cultured in their correct anatomical positions. Success of the technique appears dependent on the use of culture plate inserts which prevent cellular attachment to the plastic culture surface and the resulting migration of neurons and hair cells (HCs). Results Using this technique, we have noted an average of 5–10 neurites per SG explant growing into the oC via the spiral lamina, following the anatomic pathway used during development. Confocal microscopy was used to visualize the contact area between dendritic growth and HCs. This demonstrates branching of neurites to multiple inner HCs as well as some branches extending to outer HCs. This pattern is consistent with early cochlear development. In contrast, with alternate techniques, neurites followed very different paths to the oC, sometimes innervating inner hair cells from the outer hair cell side of the epithelium. Conclusion This culture system offers a unique capacity to evaluate factors affecting spiral ganglion neurite guidance via manipulation of either the oC or SG. Significance The use of separated SG and oC will allow tissue from knockout mice to be paired with wild-type tissue, to explore fundamental mechanisms involved in cochlear innervation. Clinical implications include the ability to optimize SG ingrowth to cochlear implant electrodes offering tremendous potential for improving frequency resolution and dynamic range, as well as the ability to direct SG dendrites to regenerated/transplanted HCs as such advances develop.

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22

Simmons, Dwayne D. "A transient afferent innervation of outer hair cells in the postnatal cochlea." NeuroReport 5, no. 11 (June 1994): 1309–12. http://dx.doi.org/10.1097/00001756-199406000-00003.

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23

Simmons, Dwayne D. "A transient afferent innervation of outer hair cells in the postnatal cochlea." NeuroReport 5, no. 11 (June 1994): 1309–12. http://dx.doi.org/10.1097/00001756-199406270-00003.

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24

Lyon, Michael J., and Rami N. Payman. "Comparison of the vascular innervation of the rat cochlea and vestibular system." Hearing Research 141, no. 1-2 (March 2000): 189–98. http://dx.doi.org/10.1016/s0378-5955(00)00004-6.

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25

Pillsbury, H. C., S. Pulver, V. N. Carrasco, K. Scruggs, D. Carver, L. de Serres, M. Bleynat, and J. Prazma. "Glyoxylic Acid in the Study of Autonomic Innervation in the Gerbil Cochlea." Archives of Otolaryngology - Head and Neck Surgery 118, no. 4 (April 1, 1992): 413–16. http://dx.doi.org/10.1001/archotol.1992.01880040079013.

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26

Ruggero, M. A., and N. C. Rich. "Timing of spike initiation in cochlear afferents: dependence on site of innervation." Journal of Neurophysiology 58, no. 2 (August 1, 1987): 379–403. http://dx.doi.org/10.1152/jn.1987.58.2.379.

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1. The phase of excitation of inner hair cells (IHCs) relative to basilar membrane motion has been estimated as a function of best frequency (BF) (or, equivalently, cochlear location) by recording responses to tones (100–1,000 Hz) from chinchilla cochlear afferent axons at their central exit from the internal auditory meatus. 2. The time of IHC excitation (i.e., the time of chemical transmitter release) was derived from the neural recordings at near-threshold levels by applying a correction for the latency of synaptic processes and the propagation time of action potentials. 3. The phase of basilar membrane motion at the appropriate innervation site was estimated on the basis of previously measured basilar membrane responses at a location close to the basal end of the cochlea and estimates of mechanical travel time from the basal end to the innervation site, derived from the neural latencies to intense rarefaction clicks, as a function of BF. 4. The derived near-threshold excitation of basal IHCs leads basilar membrane displacement toward scala tympani by approximately 40-60 degrees. 5. At BFs corresponding to midcochlear locations (2–6 kHz) there is an abrupt phase transition. The derived excitation for IHCs located at more apical locations (BFs large in relation to stimulus frequency) corresponds approximately to peak velocity of the basilar membrane toward scala vestibuli. 6. Although the derived response phases of apically located IHCs are consistent with intracellular recordings from IHCs, the derived near-threshold response phases of basal IHCs may be inconsistent with intracellular IHC recordings. 7. The foregoing results, based on responses of nearly 1,000 cochlear afferents to tones 100-1,000 Hz at near-threshold stimulus levels, amply confirm our previous conclusions that were based on a smaller sample of responses to very low frequency tones (less than or equal to 100 Hz): there is a spatial transition at midcochlear regions in the mode of excitation of IHCs, which does not seem to simply reflect the macromechanics of the basilar membrane. 8. It has been proposed that both the paradoxical response phases of high-BF afferents and the spatial phase transition arise from an influence of cochlear microphonics on the transmembrane potential of IHCs. The present results, which show that the spatial phase transition occurs for frequencies at least as high as 400 Hz, would appear to make such an electrical influence of outer hair cells on IHCs less likely. An alternative explanation might be that the phase transition has a mechanical basis, perhaps localized to micromechanical events in the subtectorial regio

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27

Tziridis, Konstantin, and Holger Schulze. "Preventive Effects of Ginkgo-Extract EGb 761® on Noise Trauma-Induced Cochlear Synaptopathy." Nutrients 14, no. 15 (July 22, 2022): 3015. http://dx.doi.org/10.3390/nu14153015.

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Noise trauma-induced loss of ribbon synapses at the inner hair cells (IHC) of the cochlea may lead to hearing loss (HL), resulting in tinnitus. We are convinced that a successful and sustainable therapy of tinnitus has to treat both symptom and cause. One of these causes may be the mentioned loss of ribbon synapses at the IHC of the cochlea. In this study, we investigated the possible preventive and curative effects of the Ginkgo biloba extract EGb 761® on noise-induced synaptopathy, HL, and tinnitus development in Mongolian gerbils (Meriones unguiculatus). To this end, 37 male animals received EGb 761® or placebo orally 3 weeks before (16 animals) or after (21 animals) a monaural acoustic noise trauma (2 kHz, 115 dB SPL, 75 min). Animals’ hearing thresholds were determined by auditory brainstem response (ABR) audiometry. A possible tinnitus percept was assessed by the gap prepulse inhibition acoustic startle reflex (GPIAS) response paradigm. Synaptopathy was quantified by cochlear immunofluorescence histology, counting the ribbon synapses of 15 IHCs at 11 different cochlear frequency locations per ear. We found a clear preventive effect of EGb 761® on ribbon synapse numbers with the surprising result of a significant increase in synaptic innervation on the trauma side relative to placebo-treated animals. Consequently, animals treated with EGb 761® before noise trauma did not develop a significant HL and were also less affected by tinnitus compared to placebo-treated animals. On the other hand, we did not see a curative effect (EGb 761® treatment after noise trauma) of the extract on ribbon synapse numbers and, consequently, a significant HL and no difference in tinnitus development compared to the placebo-treated animals. Taken together, EGb 761® prevented noise-induced HL and tinnitus by protecting from noise trauma-induced cochlear ribbon synapse loss; however, in our model, it did not restore lost ribbon synapses.

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28

Nitecka, Liliana M., and Hanna M. Sobkowicz. "The GABA/GAD innervation within the inner spiral bundle in the mouse cochlea." Hearing Research 99, no. 1-2 (September 1996): 91–105. http://dx.doi.org/10.1016/s0378-5955(96)00088-3.

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29

Morris, John-Clay K., Patricia E. Phelps, and Dwayne D. Simmons. "NADPH-diaphorase histochemistry reveals an autonomic-like innervation in the postnatal hamster cochlea." Journal of Comparative Neurology 412, no. 3 (September 27, 1999): 458–68. http://dx.doi.org/10.1002/(sici)1096-9861(19990927)412:3<458::aid-cne6>3.0.co;2-f.

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30

Stewart Cole, K., and Donald Robertson. "Early efferent innervation of the developing rat cochlea studied with a carbocyanine dye." Brain Research 575, no. 2 (March 1992): 223–30. http://dx.doi.org/10.1016/0006-8993(92)90083-l.

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31

Okamura, Hiro-oki, Isako Shibahara-Maruyama, Naonori Sugai, and Joe C. Adams. "Innervation of supporting cells in the guinea pig cochlea detected in bloc-surface preparations." NeuroReport 13, no. 13 (September 2002): 1585–88. http://dx.doi.org/10.1097/00001756-200209160-00002.

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32

Maison, Stéphane F., Douglas E. Vetter, and M. Charles Liberman. "A Novel Effect of Cochlear Efferents: In Vivo Response Enhancement Does Not Require α9 Cholinergic Receptors." Journal of Neurophysiology 97, no. 5 (May 2007): 3269–78. http://dx.doi.org/10.1152/jn.00067.2007.

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Outer hair cells in the mammalian cochlea receive a cholinergic efferent innervation that constitutes the effector arm of a sound-evoked negative feedback loop. The well-studied suppressive effects of acetylcholine (ACh) release from efferent terminals are mediated by α9/α10 ACh receptors and are potently blocked by strychnine. Here, we report a novel, efferent-mediated enhancement of cochlear sound-evoked neural responses and otoacoustic emissions in mice. In controls, a slow enhancement of response amplitude to supranormal levels appears after recovery from the classic suppressive effects seen during a 70-s epoch of efferent shocks. The magnitude of post-shock enhancement can be as great as 10 dB and tends to be greater for high-frequency acoustic stimuli. Systemic strychnine at 10 mg/kg eliminates efferent-induced suppression, revealing a purely enhancing effect of efferent shocks, which peaks within 5 s after efferent-stimulation onset, maintains a constant level through the stimulation epoch, and slowly decays back to baseline with a time constant of ∼100 s. In mice with targeted deletion of the α9 ACh receptor subunit, efferent-evoked effects resemble those in wild types with strychnine blockade, further showing that this novel efferent effect is fundamentally different from all cholinergic effects previously reported.

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33

Liberman, M. Charles, Leslie W. Dodds, and Sarah Pierce. "Afferent and efferent innervation of the cat cochlea: Quantitative analysis with light and electron microscopy." Journal of Comparative Neurology 301, no. 3 (November 15, 1990): 443–60. http://dx.doi.org/10.1002/cne.903010309.

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34

Whitlon, D. S., and H. M. Sobkowicz. "Patterns of hair cell survival and innervation in the cochlea of the Bronx waltzer mouse." Journal of Neurocytology 20, no. 11 (November 1991): 886–901. http://dx.doi.org/10.1007/bf01190467.

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35

Schwartz, I. R., and A. F. Ryan. "Amino acid labeling patterns in the efferent innervation of the cochlea: An electron microscopic autoradiographic study." Journal of Comparative Neurology 246, no. 4 (April 22, 1986): 500–512. http://dx.doi.org/10.1002/cne.902460407.

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Jeng, Jing‐Yi, Adam J. Carlton, Stuart L. Johnson, Steve D. M. Brown, Matthew C. Holley, Michael R. Bowl, and Walter Marcotti. "Biophysical and morphological changes in inner hair cells and their efferent innervation in the ageing mouse cochlea." Journal of Physiology 599, no. 1 (November 17, 2020): 269–87. http://dx.doi.org/10.1113/jp280256.

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Pamulova, Lucia, Birgitta Linder, and Helge Rask-Andersen. "Innervation of the Apical Turn of the Human Cochlea: A Light Microscopic and Transmission Electron Microscopic Investigation." Otology & Neurotology 27, no. 2 (February 2006): 270–75. http://dx.doi.org/10.1097/01.mao.0000187239.56583.d2.

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38

Furness, David N., and D. Maxwell Lawton. "Comparative Distribution of Glutamate Transporters and Receptors in Relation to Afferent Innervation Density in the Mammalian Cochlea." Journal of Neuroscience 23, no. 36 (December 10, 2003): 11296–304. http://dx.doi.org/10.1523/jneurosci.23-36-11296.2003.

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39

Karnes, Hope Elizabeth, Peter Nicholas Scaletty, and Dianne Durham. "Histochemical and Fluorescent Analyses of Mitochondrial Integrity in Chick Auditory Neurons following Deafferentation." Journal of the American Academy of Audiology 21, no. 03 (March 2010): 204–18. http://dx.doi.org/10.3766/jaaa.21.3.9.

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Abstract:

Background: Neurons rely exclusively on mitochondrial oxidative phosphorylation to meet cellular energy demands, and disruption of mitochondrial function often precipitates neuronal cell death. Auditory neurons in the chick brain stem (n. magnocellularis [NM]) receive glutamatergic innervation exclusively from ipsilateral eighth nerve afferents. Cochlea removal permanently disrupts afferent support and ultimately triggers apoptotic cell death in 30–50% of ipsilateral, deafferented neurons. Here, we evaluated whether disruption of mitochondrial function occurs during deafferentation-induced neuronal cell death. Purpose: To determine whether mitochondrial dysfunction occurs preferentially within dying NM neurons. Research Design: An experimental study. All birds underwent unilateral cochlea removal. Normally innervated neurons contralateral to surgery served as within-animal controls. Study Sample: Hatchling broiler chickens between 8 and 12 days of age served as subjects. A total of 62 birds were included in the study. Intervention: Cochlea removal was performed to deafferent ipsilateral NM neurons and trigger neuronal cell death. Data Collection and Analysis: Following unilateral cochlea removal, birds were sacrificed 12, 24, 48, or 168 hours later, and brain tissue was harvested. Brainstems were sectioned through NM and evaluated histochemically for oxidative enzyme reaction product accumulation or reacted for Mitotracker Red, an indicator of mitochondrial membrane potential (m) and cytoplasmic TdT-mediated dUTP Nick-End Labeling (TUNEL), an indicator of cell death. Histochemical staining intensities for three mitochondrial enzymes, succinate dehydrogenase (SDH), cytochrome c oxidase (CO), and ATP synthase (ATPase) were measured in individual neurons and compared in ipsilateral and contralateral NM. Comparisons were made using unpaired t-tests (CO) or Kruskal Wallis one way ANOVA followed by Dunn's post hoc pairwise comparisons (ATPase, SDH). Mitotracker Red tissue was examined qualitatively for the presence of and extent of colocalization between Mitotracker Red and TUNEL label in NM. Results: Results showed global upregulation of all three oxidative enzymes within deafferented NM neurons compared to contralateral, unperturbed NM neurons. In addition, differential SDH and ATPase staining intensities were detected across neurons within the ipsilateral nucleus, suggesting functional differences in mitochondrial metabolism across deafferented NM. Quantitative analyses revealed that deafferented neurons with preferentially elevated SDH and ATPase activities represent the subpopulation destined to die following cochlea removal. In addition, Mitotracker Red accumulated intensely within the subset of deafferented NM neurons that also exhibited cytoplasmic TdT-mediated dUTP Nick-End Labeling (TUNEL) and subsequently died. Conclusions: Taken together, our results demonstrate that a subset of deafferented NM neurons, presumably those that die, preferentially upregulates SDH, perhaps via the tricarboxylic acid (TCA) cycle. These same neurons undergo ATPase uncoupling and an eventual loss of Δψm.

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Reuss, Stefan, Daniel Balmaceda, Mirra Elgurt, and Randolf Riemann. "Neuronal Cytoglobin in the Auditory Brainstem of Rat and Mouse: Distribution, Cochlear Projection, and Nitric Oxide Production." Brain Sciences 13, no. 1 (January 5, 2023): 107. http://dx.doi.org/10.3390/brainsci13010107.

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Cytoglobin (Cygb), a hemoprotein of the globin family, is expressed in the supportive tissue cells of the fibroblast lineage and in distinct neuronal cell populations. The expression pattern and regulatory parameters of fibroblasts and related cells were studied in organs such as the kidney and liver in a variety of animal models. In contrast, knowledge about cytoglobin-expressing neurons is sparse. Only a few papers described the distribution in the brain as ubiquitous with a restricted number of neurons in focal regions. Although there is evidence for cytoglobin involvement in neuronal hypoxia tolerance, its presence in the auditory system was not studied despite high metabolism rates and oxygen demands of the cochlea and related brainstem centers. In a continuation of a previous study demonstrating Cygb-neurons in, inter alia, auditory regions of the mouse brain, we concentrated on the superior olivary complex (SOC) in the present study. We sought to investigate the distribution, projection pattern and neurochemistry of Cygb-neurons in the SOC. We conducted immunohistochemistry using a Cygb antibody and found that this brainstem region, functionally competent for bilateral hearing and providing cochlear hair cell innervation, contains a considerable number of Cygb-expressing neurons (averaging 2067 ± 211 making up 10 ±1% percent of total neuron number) in rats, and 514 ± 138 (6 ± 1%) in mice. They were observed in all regions of the SOC. Retrograde neuronal tract tracing with Fluorogold injected into the cochlea demonstrated that 1243 ± 100 (6 ± 1% of total neuron number in rat SOC)) were olivocochlear neurons. Approximately 56% of total Cygb neurons were retrogradely labelled, while the majority of olivocochlear neurons of both lateral and medial systems were Cygb-immunoreactive. We also conducted double immunofluorescence staining for Cygb and neuronal nitric oxide synthase (nNOS), the enzyme responsible for nitric oxide production, and observed that cytoglobin in the SOC frequently co-localized with nNOS. Our findings suggest that cytoglobin plays an important physiologic role in the oxygen homeostasis of the peripheral and central auditory nervous system. Further studies, also including transgenic animal models, are required to shed more light on the function(s) of Cygb in neurons, in particular of the auditory system.

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Bardhan, Tanaya, Jing‐Yi Jeng, Marco Waldmann, Federico Ceriani, Stuart L. Johnson, Jennifer Olt, Lukas Rüttiger, Walter Marcotti, and Matthew C. Holley. "Gata3 is required for the functional maturation of inner hair cells and their innervation in the mouse cochlea." Journal of Physiology 597, no. 13 (May 28, 2019): 3389–406. http://dx.doi.org/10.1113/jp277997.

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Ofsie, Michael S., Anne K. Hennig, Elizabeth P. Messana, and Douglas A. Cotanche. "Sound damage and gentamicin treatment produce different patterns of damage to the efferent innervation of the chick cochlea." Hearing Research 113, no. 1-2 (November 1997): 207–23. http://dx.doi.org/10.1016/s0378-5955(97)00150-0.

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Hemond, Sharon G., and D. Kent Morest. "Formation of the cochlea in the chicken embryo: sequence of innervation and localization of basal lamina-associated molecules." Developmental Brain Research 61, no. 1 (July 1991): 87–96. http://dx.doi.org/10.1016/0165-3806(91)90117-2.

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44

Harley, Randall J., Joseph P. Murdy, Zhirong Wang, Michael C. Kelly, Tessa-Jonne F. Ropp, Sehoon H. Park, Patricia F. Maness, Paul B. Manis, and Thomas M. Coate. "Neuronal cell adhesion molecule (NrCAM) is expressed by sensory cells in the cochlea and is necessary for proper cochlear innervation and sensory domain patterning during development." Developmental Dynamics 247, no. 7 (April 10, 2018): 934–50. http://dx.doi.org/10.1002/dvdy.24629.

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45

Fechner, Frank P., Joseph B. Nadol, Barbara J. Burgess, and M. Christian Brown. "Innervation of supporting cells in the apical turns of the guinea pig cochlea is from type II afferent fibers." Journal of Comparative Neurology 429, no. 2 (2000): 289–98. http://dx.doi.org/10.1002/1096-9861(20000108)429:2<289::aid-cne9>3.0.co;2-z.

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46

Schimmang, T., L. Minichiello, E. Vazquez, I. San Jose, F. Giraldez, R. Klein, and J. Represa. "Developing inner ear sensory neurons require TrkB and TrkC receptors for innervation of their peripheral targets." Development 121, no. 10 (October 1, 1995): 3381–91. http://dx.doi.org/10.1242/dev.121.10.3381.

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The trkB and trkC genes are expressed during the formation of the vestibular and auditory system. To elucidate the function of trkB and trkC during this process, we have analysed mice carrying a germline mutation in the tyrosine kinase catalytic domain of these genes. Neuroanatomical analysis of homozygous mutant mice revealed neuronal deficiencies in the vestibular and cochlear ganglia. In trkB (−/−) animals vestibular neurons and a subset of cochlear neurons responsible for the innervation of outer hair cells were drastically reduced. The peripheral targets of the respective neurons showed severe innervation defects. A comparative analysis of ganglia from trkC (−/−) mutants revealed a moderate reduction of vestibular neurons and a specific loss of cochlear neurons innervating inner hair cells. No nerve fibres were detected in the sensory epithelium containing inner hair cells. A developmental study of trkB (−/−) and trkC (−/−) mice showed that some vestibular and cochlear fibres initially reached their peripheral targets but failed to maintain innervation and degenerated. TrkB and TrkC receptors are therefore required for the survival of specific neuronal populations and the maintenance of target innervation in the peripheral sensory system of the inner ear.

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Manley, Geoffrey A., Christiane Haeseler, and Jutta Brix. "Innervation patterns and spontaneous activity of afferent fibres to the lagenar macula and apical basilar papilla of the chick's cochlea." Hearing Research 56, no. 1-2 (November 1991): 211–26. http://dx.doi.org/10.1016/0378-5955(91)90172-6.

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48

Eybalin, M., G. Charachon, and N. Renard. "Dopaminergic lateral efferent innervation of the guinea-pig cochlea: Immunoelectron microscopy of catecholamine-synthesizing enzymes and effect of 6-hydroxydopamine." Neuroscience 54, no. 1 (May 1993): 133–42. http://dx.doi.org/10.1016/0306-4522(93)90389-w.

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Kaiser, Alexander, Olga Alexandrova, and Benedikt Grothe. "Urocortin-expressing olivocochlear neurons exhibit tonotopic and developmental changes in the auditory brainstem and in the innervation of the cochlea." Journal of Comparative Neurology 519, no. 14 (July 27, 2011): 2758–78. http://dx.doi.org/10.1002/cne.22650.

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Graham, C. E., and D. E. Vetter. "The Mouse Cochlea Expresses a Local Hypothalamic-Pituitary-Adrenal Equivalent Signaling System and Requires Corticotropin-Releasing Factor Receptor 1 to Establish Normal Hair Cell Innervation and Cochlear Sensitivity." Journal of Neuroscience 31, no. 4 (January 26, 2011): 1267–78. http://dx.doi.org/10.1523/jneurosci.4545-10.2011.

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