Relevant bibliographies by topics / Ganglion spiral

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Ganglion spiral'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Ganglion spiral"

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Cho, Chang Hyun. "Survival of Spiral Ganglion." Korean Journal of Otorhinolaryngology-Head and Neck Surgery 52, no. 11 (2009): 869. http://dx.doi.org/10.3342/kjorl-hns.2009.52.11.869.

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Anniko, M., W. Arnold, T. Stigbrand, and A. Ström. "The Human Spiral Ganglion." ORL 57, no. 2 (1995): 68–77. http://dx.doi.org/10.1159/000276714.

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Whitlon, Donna S. "Introduction: Spiral ganglion neurons." Hearing Research 278, no. 1-2 (August 2011): 1. http://dx.doi.org/10.1016/j.heares.2011.06.005.

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Xu, Helen, Natasha Pollak, Sebahattin Cureoglu, and Michael M. Paparella. "S240 – Human Cochlear Implant Histopathology." Otolaryngology–Head and Neck Surgery 139, no. 2_suppl (August 2008): P155. http://dx.doi.org/10.1016/j.otohns.2008.05.415.

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Objectives 1) To exam the histopathology of multichannel cochlear implant temporal bones. 2) To evaluate the relationship of residual spiral ganglion cell counts to clinical hearing performance. Methods 8 temporal bones from 4 cochlear implant patients were examined histologically. Paired comparisons were made between implanted and nonimplanted temporal bones. Clinical performance data was obtained from patient charts. Results There were varying amounts of inflammation (fibrosis and ossification) in the basal turn of the cochlear in all implanted temporal bones. Trauma to the facial nerve at facial recess site was noticed in 1 case. Compared with nonimplanted ears, 2 implanted bones with less than 10-year duration of implantation had no significant changes of spiral ganglion cell population. One case with prolong implant duration (15 years) showed about 36% decrease of spiral ganglion cells at the implanted site. The case with best speech recognition (89% with CID sentence) had the highest residual spiral ganglion cells (30% of normal spiral ganglion cell population). 2 cases with poor clinical performance (< 10% with CID sentence) had the residual spiral ganglion cells at 11% and 22%. The case with moderate clinical performance (30% with CID sentence) had 14% of normal spiral ganglion cell population. Surviving dendrites varied from 5% to 30% among 4 cases with no relationship to clinical performance. Conclusions Our findings suggest prolonged implantation may affect spiral ganglion cell population. There is no reverse relationship between residual spiral ganglion cells in implanted temporal bones to clinical speech performance observed from our limited cases.
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Ariyasu, Laurence, Frank R. Galey, Raymond Hilsinger, and Frederick M. Byl. "Computer-Generated Three-Dimensional Reconstruction of the Cochlea." Otolaryngology–Head and Neck Surgery 100, no. 2 (February 1989): 87–91. http://dx.doi.org/10.1177/019459988910000201.

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Computer-generated three-dimensional reconstructions of the nerve fibers from the organ of Corti to the spiral ganglion were used to determine the optimum maximal length of the cochlear implant electrode. The spiral ganglion within the modiolus is much shorter than the organ of Corti. The spiral ganglion has turns and reaches no higher than the middle of the second turn of the organ of Corti, which has turns. The spiral ganglion is concentric and basal with respect to the organ of Corti. The spiral ganglion dendrites within the osseous spiral lamina of the basal turn project radially, nearly perpendicular to the central axis of the modiolus. Upon entering the modiolus, they turn basally at an angle of approximately 120 degrees. The projection of dendrites within the osseous spiral lamina became increasingly oblique as the ganglion extended apically. The organization of the cochlear nerve results from the spiraling of the ganglion. These findings are in agreement with previous reports. Implications of these findings and their possible relevance to the optimum length of the cochlear implant electrode are discussed with reference to cochlear damage resulting from longer electrodes.
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Khan, Aayesha M., Ophir Handzel, Donald K. Eddington, Doris Damian, and Joseph B. Nadol. "Effect of Cochlear Implantation on Residual Spiral Ganglion Cell Count as Determined by Comparison with the Contralateral Nonimplanted Inner Ear in Humans." Annals of Otology, Rhinology & Laryngology 114, no. 5 (May 2005): 381–85. http://dx.doi.org/10.1177/000348940511400508.

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It is generally assumed that at least a minimal number of spiral ganglion cells is essential for successful speech perception with a cochlear implant. Although the insertion of a multichannel cochlear implant frequently results in loss of residual hearing in the implanted ear, this outcome does not imply that significant damage to residual populations of spiral ganglion cells has occurred. The purpose of the current study was to compare spiral ganglion cell counts in implanted and nonimplanted cochleas in 11 patients for whom both temporal bones were available and in whom a multichannel cochlear implant had been placed unilaterally. The temporal bones were processed for light microscopy by standard techniques. The cochleas were reconstructed by 2-dimensional methods. Spiral ganglion cell counts of the implanted and nonimplanted sides were compared by a paired t-test (2-tailed). The mean spiral ganglion cell counts for implanted and nonimplanted ears were not statistically different in the most basal three segments of the cochlea. However, the mean spiral ganglion cell count in segment 4 (apical segment) and the mean total spiral ganglion cell count were lower in the implanted cochleas than in the nonimplanted cochleas (p < .01). The results of this study suggest a modest decrease in the total spiral ganglion cell count in the implanted ears as compared to the nonimplanted ears, principally in the apical segment. Possible interpretations of this finding are discussed.
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Chiong, Charlotte M., Robert J. Glynn, Wen-Zhuang Xu, and Joseph B. Nadol. "Survival of Scarpa's Ganglion in the Profoundly Deaf Human." Annals of Otology, Rhinology & Laryngology 102, no. 6 (June 1993): 425–28. http://dx.doi.org/10.1177/000348949310200603.

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The electrically evoked auditory brain stem response in some cochlear implant patients may be confounded by evoked potentials generated by vestibular neurons. The magnitude of this contribution to the response from the vestibular system is unknown, in part because the survival of cells within Scarpa's ganglion in profoundly deaf humans is unknown. Therefore, we undertook a quantitative study of Scarpa's ganglion in 48 deaf subjects who in life would have been candidates for cochlear implantation and in 5 subjects with normal hearing. The numbers of residual cells in both Scarpa's ganglion and the spiral ganglion in deaf subjects were significantly less than in individuals with normal hearing. Bivariate analysis demonstrated a highly significant positive correlation between cell counts of Scarpa's ganglion and the spiral ganglion. The durations of hearing loss and of profound deafness were negatively correlated with Scarpa's ganglion cell counts. However, in contrast to spiral ganglion cell survival, the cause of profound deafness did not predict the number of Scarpa's ganglion cells. Multiple linear regression analysis using a variety of clinical parameters demonstrated that the best predictor of the number of Scarpa's ganglion cells in profoundly deaf humans was the number of remaining spiral ganglion cells.
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Ramku, Emina, Refik Ramku, Dugagjin Spanca, and Valbona Zhjeqi. "Functional Pattern of Increasing Concentrations of Brain-Derived Neurotrophic Factor in Spiral Ganglion: Implications for Research on Cochlear Implants." Open Access Macedonian Journal of Medical Sciences 5, no. 2 (February 27, 2017): 121–25. http://dx.doi.org/10.3889/oamjms.2017.017.

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BACKGROUND: As previously various studies have suggested application of brain-derived neurotrophic factor (BDNF) may be considered as a promising future therapy for hearing deficits, in particular for the improvement of cochlear neurone loss during cochlear implantation.AIM: The present study's aim was to establish the upper threshold of the concentration of BDNF in Naval Medical Research Institute (NMRI) mice spiral ganglion outgrowth.METHODS: Spiral ganglion explants were prepared from post-natal day 4 (p4) (NMRI) mice of both sexes under the approval and guidelines of the regional council of Hearing Research Institute Tubingen.RESULTS: Spiral ganglion explants were cultured at postnatal days 4 in the presence of different concentrations of BDNF as described under methods. We chose an age of postnatal day (P4) and concentrations of BDNF 0; 6; 12.5; 25 and 50 ƞg/ml. Averaged neurite outgrowth is measured in 4 different cultures that were treated with different concentrations. Results show that with increasing concentrations of BDNF, the neurite density increases.CONCLUSION: The present finding show evidence that BDNF has a clear incremental effect on the number of neurites of spiral ganglia in the prehearing organ, but less on the neurite length. The upper threshold of exogenous BNDF concentration on spiral ganglion explant is 25 ƞg/ml. This means that concentration beyond this level has no further incremental impact. Therefore our suggestion for hydrogel concentration in NMRA mice in future research should be 25 ƞg/ml.
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Yilmaz-Bayraktar, Suheda, Jana Schwieger, Verena Scheper, Thomas Lenarz, Ulrike Böer, Michaela Kreienmeyer, Mariela Torrente, and Theodor Doll. "Decellularized equine carotid artery layers as matrix for regenerated neurites of spiral ganglion neurons." International Journal of Artificial Organs 43, no. 5 (August 22, 2019): 332–42. http://dx.doi.org/10.1177/0391398819868481.

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Today’s best solution in compensating for sensorineural hearing loss is the cochlear implant, which electrically stimulates the spiral ganglion neurons in the inner ear. An optimum hearing impression is not ensured due to, among other reasons, a remaining anatomical gap between the spiral ganglion neurons and the implant electrodes. The gap could be bridged via pharmacologically triggered neurite growth toward the electrodes if biomaterials for neurite guidance could be provided. For this, we investigated the suitability of decellularized tissue. We compared three different layers (tunica adventitia, tunica media, and tunica intima) of decellularized equine carotid arteries in a preliminary approach. Rat spiral ganglia explants were cultured on decellularized equine carotid artery layers and neurite sprouting was assessed quantitatively. Generally, neurite outgrowth was possible and it was most prominent on the intima (in average 83 neurites per spiral ganglia explants, followed by the adventitia (62 neurites) and the lowest growth on the media (20 neurites). Thus, decellularized equine carotid arteries showed promising effects on neurite regeneration and can be developed further as efficient biomaterials for neural implants in hearing research.
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Nadol, Joseph B., Yi-Shyang Young, and Robert J. Glynn. "Survival of Spiral Ganglion Cells in Profound Sensorineural Hearing Loss: Implications for Cochlear Implantation." Annals of Otology, Rhinology & Laryngology 98, no. 6 (June 1989): 411–16. http://dx.doi.org/10.1177/000348948909800602.

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Ninety-three temporal bones from 66 patients who were profoundly deaf during life were reconstructed by analysis of serial light microscopic sections. The correlations of total and segmental spiral ganglion cell counts with age, duration of hearing loss and profound deafness, and cause of hearing loss were evaluated. Bivariate analysis demonstrated that total spiral ganglion cell count tended to be lower in older than in younger deaf individuals and lower with longer duration of hearing loss and total deafness. However, multiple regression analysis demonstrated that the cause of hearing loss was the single most significant determinant of total spiral ganglion cell count. Patients with deafness due to aminoglycoside toxicity or sudden idiopathic deafness had the highest residual spiral ganglion cell count and patients with deafness due to presumptive postnatal viral labyrinthitis, bacterial labyrinthitis, and congenital or genetic causes had the lowest numbers of residual spiral ganglion cells.
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Dissertations / Theses on the topic "Ganglion spiral"

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Tylstedt, Sven. "The Human Spiral Ganglion." Doctoral thesis, Umeå University, Clinical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-77.

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Our knowledge of the fine structure of the Human Spiral Ganglion (HSG) is still inadequate and new treatment techniques for deafness using electric stimulation, call for further information and studies on the neuronal elements of the human cochlea. This thesis presents results of analyses of human cochlear tissue and specimens obtained during neurosurgical transpetrosal removal of life-threatening meningeomas. The use of surgical biopsies produced a well-preserved material suitable for ultrastructural and immunohistochemical studies on the human inner ear. The SG was studied with respect to fine structure, using TEM technique and the immunostaining pattern of synaptophysin, which is an integral membrane protein of neuronal synaptic vesicles. The immunostaining patterns of the tight junctional protein ZO-1 and the gap junctional proteins Cx26 and Cx43 in the human cochlea were also studied. The ultrastructural morphology revealed an absence of myelination pattern in the HSG, thus differing from that in other species. Furthermore, formation of structural units as well as signs of neural interaction between the type 1 neurons could be observed. Type 1 cells were tightly packed in clusters, sharing the ensheathment of Schwann cells. The cells frequently made direct physical contact in Schwann cell gaps in which membrane specializations appeared. These specializations consisted of symmetrically or asymmetrically distributed filamentous densities along the apposed cell membranes. The same structures were also present between individual unmyelinated nerve fibres and the type 1 cells. Synapses were observed on the type 2 neurons, with nerve fibres originating from the intraganglionic spiral bundle. Such synapses, though rare, were also observed on the type 1 cells. The ultrastructural findings were confirmed by the synaptophysin study. A 3-D model of a Schwann cell gap between two type 1 cells was constructed, describing the distribution pattern of membrane specializations. In the immunohistochemical studies on the human cochlea, ZO-1 was expressed in tissues lining scala media, thus contributing to the formation of a closed compartment system, important for the maintenance of the specific ionic composition of the endolymph. Protein Cx26 could be identified in non-sensory epithelial cells of the organ of Corti, in connective tissue cells of the spiral ligament and spiral limbus, as well as in the basal and intermediate cell layers of stria vascularis. Cx26 in this region may be involved in the recycling of potassium. Protein Cx43 stained weakly in the spiral ligament, but intense staining in the SG may indicate that gap junctions exist between these neurons. A different functional role for the HSG can be assumed from the morphological characteristics and the signs of a neural interaction between the SG cells. This might be relevant for neural processing mechanisms in speech coding and could have implications for cochlear implant techniques.

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Bailey, Erin M. "Why do spiral ganglion neurons die after deafening?" Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/4568.

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Hair cells, the auditory sensory cells, are the sole afferent input to the spiral ganglion neurons (SGNs). HCs and adjacent organ of Corti supporting cells provide neurotrophic factors that prevent SGN degeneration. Following loss of hair cells, SGNs degenerate and gradually die. Most deafness, whether congenital, age-related, or due to noise, disease, trauma, or ototoxin, is a consequence of hair cell loss. Cochlear implants, the only means of restoring hearing to deaf people, electrically stimulate the SGNs, replacing the sensory function of hair cells. SGN degeneration compromises the efficacy of cochlear implants. For example, degeneration of the peripheral process raises the threshold for electrical stimulation, necessitating higher currents that reduce battery life and, by stimulating SGNs in a larger volume, reduce the precision of frequency representation. The goal of my research is to determine why SGNs degenerate or die so that therapies can be developed to prevent it. My approach to this goal focuses on answering two significant questions. First, because the death of SGNs does not occur immediately after hair cell loss implies that hair cells are not the sole source of neurotrophic support for SGNs. Some neurotrophic support must be available even after hair cells are gone. What are the sources of neurotrophic factors for SGNs after hair cells are lost and why are they ultimately insufficient to prevent SGN death? In Chapter II I answer this question by quantifying neurotrophic factor expression in regions accessible to the SGNs: the organ of Corti and the cochlear nucleus. Answering this question will identify the key endogenous factors that support SGNs, which will facilitate development of optimal therapies. Second, the fact that SGNs die over a long period of time raises the possibility that there is a difference between SGNs that die early and those that die weeks or months later. Is the time a cell dies purely stochastic or is there something distinctive about cells that die at different times? In Chapter III, I use microarray-based gene expression profiling to compare the initial population of SGNs at the onset of SGN death to a population of SGNs still surviving at a time when about half of the SGNs have already died. Identifying distinctive molecular features in the population of cells that can survive longer in the absence of hair cells may suggest therapeutic approaches to preventing SGN degeneration or death. Finally, Chapter IV addresses some of the molecular features identified by the microarray-based profiling by examining their role in SGN degeneration.
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Huang, Jie. "Depolarization-dependent pro-survival signaling in spiral ganglion neurons." Diss., University of Iowa, 2007. https://ir.uiowa.edu/etd/214.

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Membrane depolarization is an effective neurotrophic stimulus, with its trophic effect on spiral ganglion neurons (SGNs) even surpassing that of neurotrophins. Thus, SGN cultures are a favorable system to investigate pro-survival signal transduction downstream of depolarization. Depolarization promotes SGN survival by recruiting three distinct kinase pathways: cyclic AMP-dependent protein kinase (PKA), Ca2+/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV. CaMKIV mediates the pro-survival effect of depolarization by activating CREB in nucleus. However, the mechanisms by which PKA and CaMKII promote survival are still not clear. By targeting constitutively active PKA or a PKA inhibitor (PKI) to the outer mitochondrial membrane (OMM), we showed that PKA activity at the OMM is sufficient to support SGN survival in the absence of other trophic factors and necessary for cAMP-dependent SGN survival. It has been suggested that PKA can promote survival by inactivating pro-apoptotic protein Bad. By cotransfection of SGNs with OMM-PKA and wild-type Bad, we showed that this was the case. We further showed that Ser112 and Ser136 in Bad, but not Ser155, a hypothetical PKA target, were necessary for functional inactivation of Bad by PKA. CaMKII mediates the third depolarization-dependent pro-survival pathway. A specific pro-survival target for CaMKII was identified through a separate investigation of the pro-apoptotic JNK-Jun signaling pathway, which we had identified as active in apoptotic SGNs in vivo. By measuring anti-phosphoJun immunofluorescence, we could quantify JNK-Jun activation in SGNs under different conditions. We showed that JNK inhibition or genetic deletion of JNK3 reduces SGN death after neurotrophic factor withdrawal. Neurotrophins have been shown to suppress JNK activation via their receptor protein tyrosine kinases (PTKs). By expressing constitutively active and dominant negative forms of candidate protein kinases, we identified a novel signaling pathway linking depolarization to JNK: Ca2+ entry - CaMKII - FAK/Pyk2 - PI-3-OH Kinase - Protein Kinase B - inhibition of MLKs (upstream activators of JNK). Thus, depolarization also recruits PTKs - the nonreceptor PTKs FAK and Pyk2 - to suppress JNK activation, implying a conserved PTK-PI3K-PKB pathway for suppression of pro-apoptotic JNK activation by neurotrophic stimuli.
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Galindo, Ramon Gustavo. "The effect of neurotrophic factors on spiral ganglion neurons." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/3456.

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The current study investigates the survival and neuritogenic effects of various neurotrophic factors on rat spiral ganglion neurons (SGNs) in vitro. In particular, ciliary neurotrophic factor (CNTF), glial derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3) and neurturin (NRTN) were assayed on postnatal day 4-6 SGNs. CNTF and NT-3 produced a robust survival effect while GDNF and NRTN failed to do so. A dose response revealed CNTF to be effective at promoting survival as low as 5ng/ml. In addition, CNTF promoted neurite growth in both depolarizing and non-depolarizing conditions, suggesting that CNTF can partially overcome the inhibitory effect of membrane depolarization. Lastly, the effect of NTFs was assayed between basal and apical neurons in culture. The preliminary results suggest there is no difference in response to NTFs between these two spatially distinct populations, however, it was noted that under depolarizing conditions apical neurons produce significantly shorter neurites than their basal counterparts.
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Zabalawi, Hassan A. "Spiral ganglion neurite outgrowth and pathfinding on electrospun microfibrous piezoelectric nanocomposite polymer scaffolds." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10061643/.

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Sensorineural hearing loss (SNHL) can be caused by hair cell loss and spiral ganglion neurone (SGN) degeneration. Cochlear implants (CIs), the only means of restoring residual hearing to profoundly deaf people, stimulate possible preserved SGNs electrically. Thus, SGN degeneration dictates the efficacy of CIs. SGN degeneration reduces sensitivity and frequency selectivity. In addition, stimulation thresholds increase due to SGN degeneration consequently increasing power demands. The replacement of auditory neurones with proper functional spatial alignment is an important step in the attempt to restore auditory function. This study adopts a tissue-engineering approach. We examined the viability of polyvinylidene fluoride (PVDF) and polyvinylidene trifluoroethylene (P(VDF-TrFE)). P(VDF-TrFE) was chosen to add directional growth cues through electrospinning aligned microfibrous scaffolds. The effects of the scaffolds on the length and orientation of re-growing SGN neurites and glia were tested in vitro using primary murine cultures. Two methods of SGN preparation were compared; explants and dissociated cultures. Primary SGNs showed preferential affinity to P(VDF-TrFE) microfibres and the microfibrous scaffolds were found to promote aligned SGN neurite regrowth compared to glass coverslips. Subsequently, we doped the electrospun P(VDF-TrFE) microfibres with carbon nanotubes (CNT) to optimise the scaffold mechanically and electrically. The CNT addition was found to be biocompatible and promoted aligned SGN neurite regrowth. The CNT doping enhanced the mechanical properties of the microfibres and improved scaffold handling. Moreover, the scaffolds could be biofunctionalized with neurone modulating drugs. Preliminary testing of gamma-secretase inhibitor (LY411575) showed promising regenerative effects on SGNs in vitro. In conclusion, electrospun aligned microfibrous P(VDF-TrFE)-CNT nanocomposite scaffolds can modulate glial and SGN neurite and axon organization in vitro. Combined with a specific protocol of electrical induction in the first weeks of implantation, the piezoelectric fibrous scaffold could significantly improve cochlear implantation results, frequency selectivity and minimize power demands.
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Browne, L. P. "An investigation of lipid modulation of low voltage activated currents in spiral ganglion neurons." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1477267/.

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Type I spiral ganglion neurons (SGNs) synapse onto cochlear inner hair cells and constitute the majority of afferent fibres in the auditory nerve (AN). Better characterisation of their biophysical properties may identify therapeutic targets for optimising AN sensitivity. This study aimed to characterise the membrane physiology underlying the firing properties of post-hearing onset SGNs and investigated whether their properties could be modified by the presence of native and synthetic lipids. In dissociated ganglionic cultures, SGNs displayed an intrinsic variation in their firing properties; this could be correlated with the magnitudes of specific membrane currents. SGNs were categorised by their response to depolarising current injection; SGNs either adapted to the stimulus rapidly, slowly or not at all. Rapid adaptation, a mechanism that preserves temporal precision throughout the auditory system, was found to be regulated by a dendrotoxin-K (DTX-K) and tityustoxin-Kα (TsTx)-sensitive low-threshold voltage-activated (LVA) K+ current, suggesting contribution by Kv1.1 and Kv1.2 subunits. As Kv1.2 channels were known to be positively modulated by membrane phosphoinositides, we investigated the influence of phosphatidylinositol-4,5- bisphosphate (PIP2) availability on SGN K+ currents. Inhibiting PIP2 production using wortmannin, or sequestration using a palmitoylated peptide (PIP2-PP), slowed or abolished adaptation in SGNs. PIP2-PP specifically reduced SGN LVA currents in a manner that was partly rescued by intracellular dialysis with diC8PIP2, a nonhydrolysable analogue of PIP2. PIP2-PP application induced similar levels of current inhibition in Kv1.1/Kv1.2 channels heterologously expressed in HEK293 cells. Accordingly, the lipid sensitivity of the Kv1.2 channel was further explored with a range of native and synthetic free fatty acids. Polyunsaturated fatty acids were found to be strong inhibitors of Kv1.2 currents, offering further potential candidates for SGN modulation. Collectively, this data identifies Kv1.1 and Kv1.2 containing K+ channels as key regulators of excitability in the AN, and potential targets for pharmacological modulation.
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Fryatt, Alistair Gordon. "Investigating voltage-gated sodium channel expression in rat spiral ganglion neurons following noise induced hearing loss." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/10207.

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Noise exposure has been shown to elevate hearing thresholds by damaging the cochlea through hair cell damage and the excitotoxic, excessive release of glutamate at the hair cell afferent spiral ganglion neuron (SGN) synapse. This excitotoxicity results in the loss of synaptic innervation of the neuron from the hair cell. In somatosensory neurons a similar axotomy results in altered voltage-gated sodium channel (Nav) expression. This study investigates whether similar changes in Nav expression occur in rat SGN following noise exposure. This study has shown the expression of Nav1.1, 1.6 and 1.7 in normal rat SGN using RT-PCR and immunohistochemistry. The noise exposure protocol, 2 sessions presenting a single tone (14.8kHz) at a modest 110dB SPL for 2 hours with 48 hours between each session, resulted with elevated hearing thresholds of the sound-exposed rats of 18±4dB and 24±3dB at 24kHz and 30kHz respectively, with insignificant elevation at frequencies below 16kHz. RT-PCR showed no additional Nav isoforms present in the sound-exposed cochlea. Quantitative PCR showed a significant decrease in Nav1.6 mRNA expression level, reduced by 56% compared to normal hearing animals. Nav1.1 mRNA was significantly reduced by 29% and Nav1.7 mRNA was elevated by 20% when compared to control cochleae. Immunohistochemistry of sound-exposed cochleae showed increased Nav1.1 staining along the peripheral processes of the SGN. Also, staining for Nav1.7 in the SGN was altered in sound-exposed rats compared to control animals, with the majority of sound-exposed animals showing an increase in darker stained neurons. Nav1.6 SGN cell body staining was not altered between sound-exposed and control neurons using immunohistochemistry. SGN cell body counting showed no decrease in neuronal number following sound exposure compared to control cochleae. These results show that Nav expression in rat SGN alters following sound exposure, which may modify neuronal function in deafened animals.
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Bertram, Sebastian Johannes [Verfasser], Stefan [Gutachter] Dazert, and Dominik [Gutachter] Brors. "Einfluss von Pleiotrophin auf das Wachstumsverhalten von Spiral Ganglion Neuronen / Sebastian Johannes Bertram ; Gutachter: Stefan Dazert, Dominik Brors ; Medizinische Fakultät." Bochum : Ruhr-Universität Bochum, 2020. http://d-nb.info/1216332975/34.

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Ishikawa, Masaaki. "Transplantation of neurons derived from human iPS cells cultured on collagen matrix into guinea-pig cochleae." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225472.

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Souchal, Marion. "Surdités cachées ; atteinte des cellules sensorielles cochléaires ou du nerf auditif ?" Thesis, Université Clermont Auvergne‎ (2017-2020), 2017. http://www.theses.fr/2017CLFAS003/document.

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Les surdités neurosensorielles sont classiquement décrites par une élévation des seuils auditifs généralement corrélée à une dégénérescence des cellules ciliées externes (CCE). Toutefois, des travaux récents sur des modèles animaux ont montré qu’un audiogramme normal pouvait être associé à des atteintes auditives périphériques. Ce travail de thèse a contribué à mieux caractériser chez des modèles murins, ces déficiences supraliminaires cachées liées d’une part, à des altérations des CCE et d’autre part, à la dégénérescence de certaines fibres nerveuses auditives. Dans la première partie de cette thèse, l’évolution des profils auditifs de souris présentant une dégénérescence accélérée des CCE, les souris de souche CD1-RjOrl : SWISS, a été caractérisée. Dans cette étude longitudinale, menée au cours du premier mois postnatal, une progressivité de la déficience auditive a été montrée. Toutefois, une discordance surprenante a été mise en évidence entre des seuils auditifs proches des valeurs normales à haute fréquence combinés à des produits de distorsions acoustiques (PDA) absents. Les courbes d’accord de masquage montrent un décalage des pointes vers les basses fréquences. Ces données indiquent que les CCE de la base ne sont plus fonctionnelles et que la perception des hautes fréquences est perturbée. Les observations en microscopie électronique à balayage ont révélé une conformation anormale de la touffe stéréociliaire des CCE au niveau de la base de la cochlée. Ces données témoignent d’une désorganisation de la tonotopie cochléaire. Dans la deuxième partie de cette thèse, l’effet de l’oxaliplatine sur la fonction auditive et sur la morphologie cochléaire a été décrit chez des souris adultes de souche CBA/J. L’oxaliplatine, un sel de platine utilisé en chimiothérapie, a de nombreux effets secondaires parmi lesquels l’apparition d’une neuropathie périphérique. À la suite d’un traitement avec cette drogue, les souris ne présentent pas d’élévation des seuils auditifs et pas d’altération de la fonction des CCE. Cependant, l’étude histologique révèle une dégénérescence surprenante des fibres auditives du ganglion spiral. Avec des tests électrophysiologiques supplémentaires, une diminution de l’amplitude du potentiel d’action composite a été mise en évidence. Le réflexe du système efférent olivocochléaire médian, évalué par un test de suppression controlatéral, semble également être diminué par le traitement. Les souris traitées avec de l’oxaliplatine constituent donc un modèle animal précieux de surdité cachée, qui demande à être mieux caractérisé. Les résultats de ces études confirment l’insuffisance de l’audiogramme pour détecter des altérations subtiles de la cochlée et montrent la nécessité d’améliorer le diagnostic de ces déficiences supraliminaires. Ainsi, les atteintes cachées des CCE peuvent être détectées par l’absence de PDA associée à des potentiels évoqués auditifs normaux et les neuropathies par des PDA présents associés à des potentiels évoqués auditifs anormaux. La combinaison de ces différents tests fonctionnels et électrophysiologiques permettrait une meilleure prise en charge des patients et une amélioration de leur qualité de vie
Sensorineural hearing loss are classically described by auditory thresholds elevation usually correlated with outer hair cells (OHC) degeneration. However, recent work on animal models has shown that normal audiogram can be associated with peripheral hearing impairments. This thesis contributed to better characterize, in mouse models, these hidden supraliminal deficiencies related on the one hand, with OHC alterations and on the other, to auditory nerve fibers degeneration. In the first part of this thesis, the auditory profiles evolution of mice exhibiting an OHC accelerated degeneration, the CD1-RjOrl: SWISS strain mice, was characterized. In this longitudinal study, conducted in the first postnatal month, a progressivity of the hearing impairment has been observed. However, a surprising discrepancy was found between high frequency hearing thresholds close to normal values associated with missing distortion product otoacoustic emission (DPOAE). The masking tuning curves dips are shifted toward low frequencies. Those data indicate that basal OHC are no longer functional and the perception of high frequencies is disrupted. Observations in scanning electron microscopy revealed an abnormal conformation of the OHC stereocilia bundles at the cochlea base. These results represent an evidence of a disorganized cochlear tonotopy. In the second part of this thesis, the effect of oxaliplatin on the auditory function and on the cochlear morphology was described in adult CBA/J strain mice. Oxaliplatin, a platinum salt used in chemotherapy, has many side effects including development of peripheral neuropathy. Following one treatment with this drug, mice did not present any hearing threshold elevation or OHC function impairment. However, the histological study reveals a surprising degeneration of the spiral ganglion cells. With additional electrophysiological tests, a decrease in the compound action potential amplitude has been demonstrated. The median olivocochlear efferent system reflex, evaluated by a contralateral suppression test, also seems to be diminished by the treatment. The mice treated with oxaliplatin, therefore constitute a precious animal model of hidden deafness, which needs to be better characterized. The results of these studies confirm the audiogram insufficiency to detect subtle cochlea alterations and reveal the need to improve supraliminal deficiencies diagnosis. Thus, hidden OHC impairments can be detected by the absence of DPOAE associated with normal auditory evoked potentials and neuropathies by the presence of DPOAE associated with abnormal auditory evoked potentials. The combination of these functional and electrophysiological tests would allow better management of patients and an improvement in their quality of life.Keywords: hidden hearing loss, CD1 mice, outer hair cells, masking tuning curves, tonotopy, oxaliplatine, spiral
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Books on the topic "Ganglion spiral"

1

Parker, Philip M., and James N. Parker. Ganglions: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Quinn, Sean David Philip. Enhanced neuronal regeneration, by retinoic acid, of murine dorsal root ganglia and of fetal murine and human spinal cord, in vitro. Ottawa: National Library of Canada, 1990.

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Kleef, Maarten van. Radiofrequency Lesions of the Dorsal Root Ganglion in the Treatment of Spinal Pain. Universitaire Pers Maasstricht, 1996.

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Wong, Stacy N., and Line G. Jacques. Neuropathic Groin Pain. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0017.

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Chronic neuropathic groin pain may be iatrogenic or posttraumatic and can be disabling or even crippling in some individuals. Patients may have significant sleep disturbances and may experience psychosocial effects along with significant physical limitations. A combination of pharmacologic treatments with physical therapy and local infiltrations may be useful. Neurostimulation techniques, including spinal cord stimulation, peripheral nerve stimulation, and dorsal root ganglion stimulation, have shown promising results in the treatment of chronic neuropathic pain. In certain cases, surgical approaches, including selective neurectomy, can be effective; in other cases, the pain will remain chronic and intractable despite all interventional measures. In summary, patients with neuropathic groin pain can be treated after a thorough pretreatment investigation. Dorsal root ganglion stimulation is a viable option and should be considered when treating this challenging patient population.
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DiMuro, John M., and Mehul J. Desai. Sympathetic Blockade of the Spine. Edited by Mehul J. Desai. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199350940.003.0030.

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This chapter focuses on the typical pain complaints and their appropriateness for sympathetic blockade and neurolysis. Anatomic considerations, block technique, associated risks, and evidence of a successful block are covered for the stellate ganglion block, T2 sympathetic block, thoracic splanchnic block, celiac plexus block, superior hypogastric plexus block, and ganglion of impar block. Sympathetic blockade is commonly used for visceral pain syndromes. Visceral pain syndromes typically are not responsive to neuraxial blocks as well as conventional rehabilitative and pharmacologic treatments. Spinal sympathetic techniques involve careful prevertebral needle placement, typically using fluoroscopic guidance. The proximity of major vessels near the target injection area is the primary risk of these techniques. In general, sympathetic blocks are non-diagnostic, but they can still help determine whether a sympathetically mediated pain condition may be present and if sympatholysis may be an effective treatment option.
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McClenahan, Maureen F., and William Beckman. Pain Management Techniques. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0011.

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This chapter provides a broad review of various interventional pain management procedures with a focus on indications, anatomy, and complications. Specific techniques reviewed include transforaminal epidural steroid injection, lumbar sympathetic block, stellate ganglion block, cervical and lumbar radiofrequency ablation, gasserian ganglion block, sacroiliac joint injection, celiac plexus block, lateral femoral cutaneous nerve block, ilioinguinal block, lumbar medial branch block, obturator nerve block, ankle block, occipital nerve block, superior hypogastric plexus block, spinal cord stimulation, and intrathecal drug delivery systems. The chapter reviews contrast agents, neurolytic agents, botulinum toxin use, corticosteroids, and ziconotide pharmacology and side effects in addition to diagnosis and management of local anesthetic toxicity syndrome. It also discusses indications for neurosurgical techniques including dorsal root entry zone lesioning. In addition, information on radiation safety and the use of anticoagulants with neuraxial blocks is covered.
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Filler, Aaron G. Piriformis Syndrome and Other Nerve Entrapments of the Posterior Pelvis. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0011.

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Not every case of neurologically based pelvic/genital numbness/incontinence is due to cauda equina syndrome. Pelvic pain, incontinence, and sexual dysfunction can result from treatable peripheral nerve injury or entrapment affecting the pudendal nerves or impar ganglion. Learning the signs, physical exam findings, tests, and surgical options greatly expands a neurosurgeon’s range. The pudendal nerve and nerve to the obturator internus muscle arise after S2, S3, and S4 spinal nerves traverse the piriformis muscle. They exit the sciatic notch with the sciatic nerve but then re-enter the pelvis, where the pudendal nerve then gives off bladder, rectal, and genital branches.
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1925-, Zenker W., and Neuhuber Winfried L, eds. The Primary afferent neuron: A survey of recent morpho-functional aspects. New York: Plenum Press, 1990.

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(Editor), Wolfgang Zenker, and Winfried L. Neuhuber (Editor), eds. The Primary Afferent Neuron: A Survey of Recent Morpho-Functional Aspects. Springer, 1990.

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Shah, Chirag D., and Maunak V. Rana. Advances in Dorsal Column Stimulation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0017.

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Spinal cord stimulation (SCS) has been a long established therapy for various pain conditions including low back pain, failed back surgery syndrome, complex regional pain syndrome, and other neuropathic and nociceptive pain states. Since the first report of SCS in 1967 by Shealy, advances have occurred in the technology used to achieve clinical analgesia. Developments in both the hardware and software involved have led to significant improvements in functional specificity, as seen in dorsal root ganglion stimulation, along with increasing breadth and depth of the field of neuromodulation. The patient experience during the implantation of the systems, as well as post-procedurally has been enhanced with improvements in programming. These technological improvements have been validated in quality evidenced-based medicine: what was a static area now is a dynamic field, with neuromodulation poised to allow physicians and patients more viable options for better pain control for chronic painful conditions.
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Book chapters on the topic "Ganglion spiral"

1

Kangelaris, Gerald T., and Lawrence R. Lustig. "Spiral Ganglion." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 2540. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_200090.

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Woodson, Erika. "Spiral Ganglion Neuron." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 2540. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_200176.

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Goodrich, Lisa V. "Early Development of the Spiral Ganglion." In The Primary Auditory Neurons of the Mammalian Cochlea, 11–48. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-3031-9_2.

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Muniak, Michael A., Catherine J. Connelly, Kirupa Suthakar, Giedre Milinkeviciute, Femi E. Ayeni, and David K. Ryugo. "Central Projections of Spiral Ganglion Neurons." In The Primary Auditory Neurons of the Mammalian Cochlea, 157–90. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-3031-9_6.

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Sekiya, Tetsuji, and Harukazu Hiraumi. "Spiral Ganglion Cell and Auditory Neuron." In Regenerative Medicine for the Inner Ear, 53–59. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54862-1_6.

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Davis, Robin L., and Robert A. Crozier. "The Electrophysiological Signature of Spiral Ganglion Neurons." In The Primary Auditory Neurons of the Mammalian Cochlea, 85–116. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-3031-9_4.

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Green, Steven H., Erin M. Bailey, Jonathan C. Kopelovich, and Marlan R. Hansen. "The Spiral Ganglion in an Out-of-Body Experience: A Brief History of in Vitro Studies of the Spiral Ganglion." In The Primary Auditory Neurons of the Mammalian Cochlea, 191–227. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-3031-9_7.

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Lee, Jeong Han, Choongryoul Sihn, Wanging Wang, Cristina Maria Perez Flores, and Ebenezer N. Yamoah. "In Vitro Functional Assessment of Adult Spiral Ganglion Neurons (SGNs)." In Methods in Molecular Biology, 513–23. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3615-1_29.

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Green, Steven H. "Neurotrophic Signaling by Membrane Electrical Activity in Spiral Ganglion Neurons." In Cell and Molecular Biology of the Ear, 165–82. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4223-0_13.

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Yamazaki, Hiroshi, and Takayuki Nakagawa. "Gene Therapy for Regeneration and Preservation of Spiral Ganglion Neurons." In Regenerative Medicine for the Inner Ear, 255–64. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54862-1_27.

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Conference papers on the topic "Ganglion spiral"

1

Diensthuber, M., J. Gabrielpillai, T. Stöver, and C. Geissler. "Normelatonin is a neuroprotective factor for postnatal spiral ganglion cells." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641041.

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Schulze, J., L. Heinkele, M. Steffens, A. Warnecke, T. Lenarz, I. Just, and A. Rohrbeck. "Rho-GTPase and p38 mediated neuroprotection in spiral ganglion cells." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641057.

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Volkenstein, S., S. Bertram, L. Roll, J. Reinhard, A. Faissner, and S. Dazert. "Pleiotrophin modulates neurite outgrowth of spiral ganglion neurons in vitro." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640663.

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Yong, J., W. G. A. Brown, K. Needham, B. A. Nayagam, A. Yu, S. L. McArthur, and P. R. Stoddart. "Dark-field microspectroscopic analysis of gold nanorods in spiral Ganglion neurons." In SPIE Micro+Nano Materials, Devices, and Applications, edited by James Friend and H. Hoe Tan. SPIE, 2013. http://dx.doi.org/10.1117/12.2033767.

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Gabrielpillai, J., C. Geissler, T. Stöver, and M. Diensthuber. "Amitriptyline increases survival rate and neurite outgrowth of spiral ganglion Neurons." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641047.

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Izawa, Masato, and Hiroyuki Torikai. "Nonlinear responses of an asynchronous cellular automaton model of spiral ganglion cell." In 2014 International Joint Conference on Neural Networks (IJCNN). IEEE, 2014. http://dx.doi.org/10.1109/ijcnn.2014.6889594.

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Wrobel, C., and D. Beutner. "Minimally invasive transcochlear approach for future optogenetic manipulation of spiral ganglion neurons." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686548.

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Lumbreras, V., E. Bas, C. Gupta, and S. M. Rajguru. "Pulsed Infrared-evoked Intracellular Calcium Transients in Neonatal Vestibular and Spiral Ganglion Neurons." In 2013 29th Southern Biomedical Engineering Conference (SBEC 2013). IEEE, 2013. http://dx.doi.org/10.1109/sbec.2013.59.

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Peter, M., U. Reich, A. Warnecke, H. Olze, A. Szczepek, T. Lenarz, and G. Paasche. "Influence of electrical stimulation on survival and growth of spiral ganglion neurons in vitro." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641053.

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Kempfle, J., C. Hamadani, N. Koen, C. McKenna, and D. Jung. "Development of a novel bisphosphonate-7,8-dihydroxyflavone (DHF) derivative for regeneration of spiral ganglion synapses." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640413.

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