Relevant bibliographies by topics / Cochlea – Innervation

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  2. Dissertations / Theses
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Academic literature on the topic 'Cochlea – Innervation'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Cochlea – Innervation"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Cochlea – Innervation"

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Brown, Daniel. "Origins and use of the stochastic and sound-evoked extracellular activity of the auditory nerve." University of Western Australia. Dept. of Physiology, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0082.

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[Truncated abstract] The present study investigated whether any of the characteristics of the compound action potential (CAP) waveform or the spectrum of the neural noise (SNN) recorded from the cochlea, could be used to examine abnormal spike generation in the type I primary afferent neurones, possibly due to pathologies leading to abnormal hearing such as tinnitus or tone decay. It was initially hypothesised that the CAP waveform and SNN contained components produced by the local action currents generated at the peripheral ends of the type I primary afferent neurones, and that changes in these local action currents occurred due to changes in the membrane potential of these neurones. It was further hypothesised that the lateral olivo-cochlear system (LOCS) efferent neurones regulate the membrane potential of the primary afferent dendrites to maintain normal action potential generation, where instability in the membrane potential might lead to abnormal primary afferent firing, and possibly one form of tinnitus. We had hoped that the activity of the LOCS efferent neurones could be observed through secondary changes in the CAP waveform and SNN, resulting from changes in the membrane potential of the primary afferent neurones. The origins of the neural activity generating the CAP waveform and SNN peaks, and the effects of the LOCS on the CAP and SNN were experimentally investigated in guinea pigs using lesions in the auditory system, transient ischemia and asphyxia, focal and systemic temperature changes, and pharmacological manipulations of different regions along the auditory pathway. ... Therefore, the CAP and SNN are altered by changes in the propagation of the action potential along the primary afferent neurones, by changes in the morphology of the tissues surrounding the cochlear nerve, and by changes in the time course of the action currents. If the CAP waveform is not altered, the amplitude of the 1kHz speak in the spontaneous SNN can be used as an objective measure of the spontaneous firing rate of the cochlear neurones. However, because the SNN contains a complex mixture of neural activity from all cochlear neurones, and the amplitude of the spontaneous SNN is variable, it would be difficult to use the spontaneous SNN alone as a differential diagnostic test of cochlear nerve pathologies. To record extratympanic electrocochleography (ET ECochG) from humans, a custom-designed, inexpensive, low-noise, optically isolated biological amplifier was built. Furthermore, a custom-designed extratympanic active electrode and ear canal indifferent electrode were designed, which increased the signal-to-noise ratio of the ECochG recording by a factor of 2, decreasing the overall recording time by 75%. The human and guinea pig CAP waveforms recorded in the present study appeared similar, suggesting that the origins of the human and guinea pig CAP waveforms were the same, and that experimental manipulations of the guinea pig CAP waveform can be used to diagnose the cause of abnormal human ECochG waveforms in cases of cochlear nerve pathologies.
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Grant, Lisa. "The role of ryanodine receptors and transient efferent innervation in cochlear inner hair cell afferent transmission." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424421.

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Safieddine, Saaid. "Etude des innervations cochléaires par immunofluorescence et par hybridation in situ : détection des récepteurs et coexistence des neurotransmetteurs/neuromodulateurs." Montpellier 2, 1993. http://www.theses.fr/1993MON20047.

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1)coexpression des recepteurs des acides amines excitateurs par les neurones auditifs primaires i. L'expression des arnm de la sous-unite glur4 etait limitee aux seules cellules gliales. Les recepteurs nmdar-1, glur2, glur3 et mglur1, sont exprimes par les neurones auditifs primairesi innervant les cellules ciliees internes. En accord avec l'implication predominante des recepteurs ampa dans la neurotransmission cochleaire, le marquage obtenu par les sous-unites glur2 et glur3 etait plus intense que pour les recepteurs nmda et mglur1. 2)coexistence de neurotransmetteurs/neuromodulateurs dans les efferences olivocochleaires. La majorite des neurones du systeme efferent lateral coexprimait les marqueurs (enzyme de synthese, arnm) de cinq substances neuroactives: l'acetylcholine, gaba, la dopamine, enkephalines, et le cgrp. Seul le gaba l'acetylcholine et le cgrp seraient co-exprimes par les neurones du systeme efferent median. 3)expression des recepteurs muscariniques m3 et dopaminergiques d1 et d2. Les neurones auditifs primaires exprimaient les arnm des recepteurs d1 et d2 et des recepteurs muscariniques m3. De plus, les arnm des recepteurs d2 et m3 etaient presents dans les neurones de l'innervation laterale. 4)excitotoxicite et plasticite neuronale. Apres episode excitotoxique par l'ampa, une perte transitoire des reponses electrophysiologiques et une surexpression des arnm des recepteurs nmda et mglur1 et des neurotransmetteurs efferents, etaient observees. La concomitance entre la reapparition des reponses cochleaires et les variations d'expression des arnm suggereraient une implication de ces recepteurs dans la restauration fonctionnelle
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Books on the topic "Cochlea – Innervation"

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Book chapters on the topic "Cochlea – Innervation"

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Kondo, Kenji, Yulian Jin, Makoto Kinoshita, Tatsuya Yamasoba, and Kimitaka Kaga. "Morphology, Development, and Neurotrophic Regulation of Cochlear Afferent Innervation." In Cochlear Implantation in Children with Inner Ear Malformation and Cochlear Nerve Deficiency, 29–46. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1400-0_4.

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Cotanche, Douglas A., and Anne K. Hennig. "Loss and Regeneration of Cochlear Hair Cell Innervation Following Sound and Drug Damage." In Cell and Molecular Biology of the Ear, 145–55. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4223-0_11.

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Fuchs, Paul Albert, Jing-jing Sherry Wu, Pankhuri Vyas, and Stephen Paul Zachary. "Cochlear Microcircuits." In Handbook of Brain Microcircuits, edited by Gordon M. Shepherd and Sten Grillner, 403–14. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190636111.003.0034.

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The mammalian cochlea functions as a sensitive frequency analyzer of the acoustic world. To a large extent, this operation is intrinsic to the peripheral organ itself, resulting from the exquisitely differentiated mechanics of the sensory epithelium that encodes sound onto cochlear afferents. The precise arrangement of afferent innervation further refines and differentiates that coding. In addition, cochlear operation is modulated by feedback from efferent neurons making contact with hair cells and afferent neurons. In this way, microcircuits of the auditory periphery involve an intricate interplay of micromechanics and cellular integration. This chapter will describe that interplay, with an emphasis on the synaptic connections of sensory hair cells with afferent and efferent neurons. To do so requires an understanding of the peripheral transduction pathway, which begins with an overview of cochlear function.
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Bauch, Christopher D., and Wayne O. Olsen. "Audiogram, Acoustic Reflexes, and Evoked Otoacoustic Emissions." In Clinical Neurophysiology, 851–59. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259631.003.0050.

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Pure-tone air-conduction and bone-conduction evaluations separate hearing loss into conductive, sensorineural, or mixed categories, and also indicate the degree of hearing loss and attendant communication difficulties. The inclusion of specific types of speech tests assess the ability of the patient to hear and understand speech. Acoustic reflex threshold and reflex decay evaluations evaluate a complex neural network, including afferent pathways to and through the lower brainstem, decussating brainstem pathways, and efferent innervation of CN VII to the stapedius muscle in the middle ear. Evoked otoacoustic emissions provide objective measurement of the peripheral auditory system coursing from the external canal to the cochlear outer hair cells. They are implemented widely in screening tests for hearing in infants, for patients suspected of auditory neuropathy spectrum disorder, and for patients suspected of pseudohypacusis; that is, feigning or exaggerated hearing loss.
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Bauch, Christopher D., and Wayne O. Olsen. "Audiogram, Acoustic Reflexes, and Evoked Otoacoustic Emissions." In Clinical Neurophysiology, 295–304. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780195385113.003.0020.

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Audiologic testing in the form of pure-tone air-conduction and bone-conduction audiograms provides diagnostic information about the type of hearing loss (conductive, sensorineural, or mixed) and the degree of hearing loss and attendant communication difficulties. The addition of speech tests that use specific types of speech stimuli directly assesses the patient’s ability to hear and to understand speech. Acoustic reflex and reflex decay tests are used to evaluate the integrity of a complicated neural network involving not only the auditory tracts to and through the brain stem but also decussating pathways in the brain stem and the course of CN VII to the innervation of the stapedius muscle. EOAE tests provide an objective measurement of the peripheral hearing system from the external ear through the cochlear outer hair cells. They are useful screening tests for hearing in infants, in patients suspected of auditory neuropathy/dys-synchrony, and in patients suspected to have pseudohypacusis, that is, feigned or exaggerated hearing loss.
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