Strenzke, Nicola

[["dc.bibliographiccitation.artnumber","e2005114"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Cruces-Solís, Hugo"],["dc.contributor.author","Jing, Zhizi"],["dc.contributor.author","Babaev, Olga"],["dc.contributor.author","Rubin, Jonathan"],["dc.contributor.author","Gür, Burak"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","de Hoz, Livia"],["dc.date.accessioned","2020-11-24T10:40:59Z"],["dc.date.available","2020-11-24T10:40:59Z"],["dc.date.issued","2018"],["dc.description.abstract","Detecting regular patterns in the environment, a process known as statistical learning, is essential for survival. Neuronal adaptation is a key mechanism in the detection of patterns that are continuously repeated across short (seconds to minutes) temporal windows. Here, we found in mice that a subcortical structure in the auditory midbrain was sensitive to patterns that were repeated discontinuously, in a temporally sparse manner, across windows of minutes to hours. Using a combination of behavioral, electrophysiological, and molecular approaches, we found changes in neuronal response gain that varied in mechanism with the degree of sound predictability and resulted in changes in frequency coding. Analysis of population activity (structural tuning) revealed an increase in frequency classification accuracy in the context of increased overlap in responses across frequencies. The increase in accuracy and overlap was paralleled at the behavioral level in an increase in generalization in the absence of diminished discrimination. Gain modulation was accompanied by changes in gene and protein expression, indicative of long-term plasticity. Physiological changes were largely independent of corticofugal feedback, and no changes were seen in upstream cochlear nucleus responses, suggesting a key role of the auditory midbrain in sensory gating. Subsequent behavior demonstrated learning of predictable and random patterns and their importance in auditory conditioning. Using longer timescales than previously explored, the combined data show that the auditory midbrain codes statistical learning of temporally sparse patterns, a process that is critical for the detection of relevant stimuli in the constant soundscape that the animal navigates through."],["dc.identifier.doi","10.1371/journal.pbio.2005114"],["dc.identifier.pmid","30048446"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69155"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Auditory midbrain coding of statistical learning that results from discontinuous sensory stimulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Rankovic, Vladan"],["dc.contributor.author","Vogl, Christian"],["dc.contributor.author","Dörje, Nele M."],["dc.contributor.author","Bahader, Iman"],["dc.contributor.author","Duque-Afonso, Carlos J."],["dc.contributor.author","Thirumalai, Anupriya"],["dc.contributor.author","Weber, Thomas"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2021-04-14T08:29:50Z"],["dc.date.available","2021-04-14T08:29:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Hearing impairment is the most common sensory disorder in humans. So far, rehabilitation of profoundly deaf subjects relies on direct stimulation of the auditory nerve through cochlear implants. However, in some forms of genetic hearing impairment, the organ of Corti is structurally intact and therapeutic replacement of the mutated gene could potentially restore near natural hearing. In the case of defects of the otoferlin gene (OTOF), such gene therapy is hindered by the size of the coding sequence (~6 kb) exceeding the cargo capacity (\\u0026lt;5 kb) of the preferred viral vector, adeno-associated virus (AAV). Recently, a dual-AAV approach was used to partially restore hearing in deaf otoferlin knock-out (Otof-KO) mice. Here, we employed in vitro and in vivo approaches to assess the gene-therapeutic potential of naturally-occurring and newly-developed synthetic AAVs overloaded with the full-length Otof coding sequence. Upon early postnatal injection into the cochlea of Otof-KO mice, overloaded AAVs drove specific expression of otoferlin in ~30% of all IHCs, as demonstrated by immunofluorescence labeling and polymerase chain reaction. Recordings of auditory brainstem responses and a behavioral assay demonstrated partial restoration of hearing. Together, our results suggest that viral gene therapy of DFNB9—using a single overloaded AAV vector—is indeed feasible, reducing the complexity of gene transfer compared to dual-AAV approaches."],["dc.identifier.doi","10.3389/fnmol.2020.600051"],["dc.identifier.pmid","33488357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83002"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/123"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","Frontiers Media S.A."],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1662-5099"],["dc.relation.workinggroup","RG Moser (Molecular Anatomy, Physiology and Pathology of Sound Encoding)"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Overloaded Adeno-Associated Virus as a Novel Gene Therapeutic Tool for Otoferlin-Related Deafness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","15"],["dc.contributor.affiliation","Stalmann, Ursula; 1Auditory Systems Physiology Group, Department of Otolaryngology and Institute for Auditory Neuroscience, SFB 889 project A06, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Franke, Albert Justin; 1Auditory Systems Physiology Group, Department of Otolaryngology and Institute for Auditory Neuroscience, SFB 889 project A06, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Al-Moyed, Hanan; 2Molecular Biology of Cochlear Neurotransmission Group, Department of Otolaryngology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Strenzke, Nicola; 1Auditory Systems Physiology Group, Department of Otolaryngology and Institute for Auditory Neuroscience, SFB 889 project A06, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Reisinger, Ellen; 2Molecular Biology of Cochlear Neurotransmission Group, Department of Otolaryngology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Stalmann, Ursula"],["dc.contributor.author","Franke, Albert Justin"],["dc.contributor.author","Al-Moyed, Hanan"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Reisinger, Ellen"],["dc.date.accessioned","2021-09-01T06:38:17Z"],["dc.date.available","2021-09-01T06:38:17Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:49Z"],["dc.description.abstract","Deficiency of otoferlin causes profound prelingual deafness in humans and animal models. Here, we closely analyzed developmental deficits and degenerative mechanisms in Otof knock-out ( Otof –/– ) mice over the course of 48 weeks. We found otoferlin to be required for proper synapse development in the immature rodent cochlea: In absence of otoferlin, synaptic pruning was delayed, and postsynaptic boutons appeared enlarged at 2 weeks of age. At postnatal day 14 (P14), we found on average ∼15 synapses per inner hair cell (IHC) in Otof –/– cochleae as well as in wild-type controls. Further on, the number of synapses in Otof –/– IHCs was reduced to ∼7 at 8 weeks of age and to ∼6 at 48 weeks of age. In the same period, the number of spiral ganglion neurons (SGNs) declined in Otof –/– animals. Importantly, we found an age-progressive loss of IHCs to an overall number of 75% of wildtype IHCs. The IHC loss more prominently but not exclusively affected the basal aspects of the cochlea. For outer hair cells (OHCs), we observed slightly accelerated age-dependent degeneration from base to apex. This was associated with a progressive decay in DPOAE amplitudes for high frequency stimuli, which could first be observed at the age of 24 weeks in Otof –/– mice. Our data will help to plan and predict the outcome of a gene therapy applied at various ages of DFNB9 patients."],["dc.description.abstract","Deficiency of otoferlin causes profound prelingual deafness in humans and animal models. Here, we closely analyzed developmental deficits and degenerative mechanisms in Otof knock-out ( Otof –/– ) mice over the course of 48 weeks. We found otoferlin to be required for proper synapse development in the immature rodent cochlea: In absence of otoferlin, synaptic pruning was delayed, and postsynaptic boutons appeared enlarged at 2 weeks of age. At postnatal day 14 (P14), we found on average ∼15 synapses per inner hair cell (IHC) in Otof –/– cochleae as well as in wild-type controls. Further on, the number of synapses in Otof –/– IHCs was reduced to ∼7 at 8 weeks of age and to ∼6 at 48 weeks of age. In the same period, the number of spiral ganglion neurons (SGNs) declined in Otof –/– animals. Importantly, we found an age-progressive loss of IHCs to an overall number of 75% of wildtype IHCs. The IHC loss more prominently but not exclusively affected the basal aspects of the cochlea. For outer hair cells (OHCs), we observed slightly accelerated age-dependent degeneration from base to apex. This was associated with a progressive decay in DPOAE amplitudes for high frequency stimuli, which could first be observed at the age of 24 weeks in Otof –/– mice. Our data will help to plan and predict the outcome of a gene therapy applied at various ages of DFNB9 patients."],["dc.identifier.doi","10.3389/fncel.2021.677543"],["dc.identifier.eissn","1662-5102"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88902"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5102"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Otoferlin Is Required for Proper Synapse Maturation and for Maintenance of Inner and Outer Hair Cells in Mouse Models for DFNB9"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","360"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Life"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Boeckhaus, Jan"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Storz, Celine"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2021-04-14T08:24:02Z"],["dc.date.available","2021-04-14T08:24:02Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/life10120360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81139"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2075-1729"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Characterization of Sensorineural Hearing Loss in Children with Alport Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e254"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Klugmann, M."],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Monasterio-Schrader, P. D."],["dc.contributor.author","Strenzke, N."],["dc.contributor.author","Flügge, G."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Pawlak, R."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2013"],["dc.description.abstract","Claustrophobia, the well-known fear of being trapped in narrow/closed spaces, is often considered a conditioned response to traumatic experience. Surprisingly, we found that mutations affecting a single gene, encoding a stress-regulated neuronal protein, can cause claustrophobia. Gpm6a-deficient mice develop normally and lack obvious behavioral abnormalities. However, when mildly stressed by single-housing, these mice develop a striking claustrophobia-like phenotype, which is not inducible in wild-type controls, even by severe stress. The human GPM6A gene is located on chromosome 4q32-q34, a region linked to panic disorder. Sequence analysis of 115 claustrophobic and non-claustrophobic subjects identified nine variants in the noncoding region of the gene that are more frequent in affected individuals (P=0.028). One variant in the 3'untranslated region was linked to claustrophobia in two small pedigrees. This mutant mRNA is functional but cannot be silenced by neuronal miR124 derived itself from a stress-regulated transcript. We suggest that loosing dynamic regulation of neuronal GPM6A expression poses a genetic risk for claustrophobia."],["dc.format.extent","12"],["dc.identifier.doi","10.1038/tp.2013.28"],["dc.identifier.gro","3150562"],["dc.identifier.pmid","23632458"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7336"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.subject","chromosome 4; GPM6A; human pedigree; miR124; mouse mutant; panic disorder"],["dc.title","A single gene defect causing claustrophobia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","40"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Reisinger, Ellen"],["dc.contributor.author","Westekemper, Katharina"],["dc.contributor.author","Ehrenreich, Ludwig"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Fischer, Julia"],["dc.date.accessioned","2017-09-07T11:47:41Z"],["dc.date.available","2017-09-07T11:47:41Z"],["dc.date.issued","2012"],["dc.description.abstract","BACKGROUND:Transgenic mice have become an important tool to elucidate the genetic foundation of the human language faculty. While learning is an essential prerequisite for the acquisition of human speech, it is still a matter of debate whether auditory learning plays any role in the development of species-specific vocalizations in mice. To study the influence of auditory input on call development, we compared the occurrence and structure of ultrasonic vocalizations from deaf otoferlin-knockout mice, a model for human deafness DFNB9, to those of hearing wild-type and heterozygous littermates.RESULTS:We found that the occurrence and structure of ultrasonic vocalizations recorded from deaf otoferlin-knockout mice and hearing wild-type and heterozygous littermates do not differ. Isolation calls from 16 deaf and 15 hearing pups show the same ontogenetic development in terms of the usage and structure of their vocalizations as their hearing conspecifics. Similarly, adult courtship 'songs' produced by 12 deaf and 16 hearing males did not differ in the latency to call, rhythm of calling or acoustic structure.CONCLUSION:The results indicate that auditory experience is not a prerequisite for the development of species-specific vocalizations in mice. Thus, mouse models are of only limited suitability to study the evolution of vocal learning, a crucial component in the development of human speech. Nevertheless, ultrasonic vocalizations of mice constitute a valuable readout in studies of the genetic foundations of social and communicative behavior."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.1186/1471-2202-13-40"],["dc.identifier.gro","3150690"],["dc.identifier.pmid","22533376"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7474"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1471-2202"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.subject","DFNB9; Evolution; Language; Mice; Ontogeny; Otoferlin; Speech; Vocal learning"],["dc.title","Mice do not require auditory input for the normal development of their ultrasonic vocalizations"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","219"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Laryngoscope Investigative Otolaryngology"],["dc.bibliographiccitation.lastpage","225"],["dc.bibliographiccitation.volume","7"],["dc.contributor.affiliation","Bevis, Nicholas F.; 1\r\nDepartment of Otorhinolaryngology, Head and Neck Surgery\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Klinge‐Strahl, Astrid; 1\r\nDepartment of Otorhinolaryngology, Head and Neck Surgery\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Strenzke, Nicola; 1\r\nDepartment of Otorhinolaryngology, Head and Neck Surgery\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Beutner, Dirk; 1\r\nDepartment of Otorhinolaryngology, Head and Neck Surgery\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.author","Wrobel, Christian"],["dc.contributor.author","Bevis, Nicholas F."],["dc.contributor.author","Klinge‐Strahl, Astrid"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Beutner, Dirk"],["dc.date.accessioned","2022-01-11T14:08:14Z"],["dc.date.available","2022-01-11T14:08:14Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T13:34:48Z"],["dc.description.abstract","Abstract Objective Evaluation of the self‐perceived hearing impairment and performance after cochlear implantation in patients with definite Menière's disease (MD). Patients and Methods Seventeen unilaterally or bilaterally profoundly hearing‐impaired patients suffering from MD who received a cochlear implantat (CI) were eligible for inclusion in this study. Their self‐perceived hearing impairment using the short Speech Spatial and Qualities of Hearing Scale (SSQ12) as well as their performance in speech perception (German language Freiburger mono‐ and multisyllable test, Oldenburger sentence test) were compared with a best‐matched control group of non‐MD patients up to 24 months of follow‐up. Results MD patients improved significantly in perception of monosyllables presented at 65 dBSPL, from preoperatively best aided 18.2% [2.4, 34.0] to 51.7% [39.4, 63.9] 1 year after cochlear implantation (mean [95% confidence interval]). Their performance approached the matched controls with 63.2% [55.7, 70.8]. Monosyllables presented at a lower intensity of 55 dBSPL revealed a significant underperformance of the MD patients (21.1% [12.6, 29.6]) in contrast to the non‐MD controls (39.1% [30.9, 47.4]) 12 months post‐CI. Self‐assessed hearing disability was significantly more pronounced in MD patients with a mean total SSQ12 score of 3.6 [2.4, 4.9] in comparison to 6.1 [5.4, 6.8] of the matched non‐MD controls after 12 months of cochlear implantation. Conclusion Cochlear implantation substantially improves hearing capabilities in profoundly hearing‐impaired patients with MD, but they tend to underperform in comparison to non‐MD patients at least at lower sound pressure levels. This is likely one reason for the poorer self‐assessed hearing function of cochlear implanted MD patients. Level of Evidence 3, retrospective, nonrandomized follow‐up study."],["dc.description.abstract","The current study evaluates self‐perceived hearing function using the SSQ12 as well as speech perception in cochlear implanted patients with Menière's disease. It reveals greater self‐assessed hearing impairment with an accompanying worse speech perception at lower sound pressure levels of Menière patients in comparison to a best‐matched control group of non‐Menière CI patients. image"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/lio2.714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97975"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2378-8038"],["dc.relation.issn","2378-8038"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Performance and self‐perceived hearing impairment after cochlear implantation in Menière's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14530"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lukashkina, Victoria A."],["dc.contributor.author","Levic, Snezana"],["dc.contributor.author","Lukashkin, Andrei N."],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Russell, Ian J."],["dc.date.accessioned","2018-11-07T10:27:16Z"],["dc.date.available","2018-11-07T10:27:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Accelerated age-related hearing loss disrupts high-frequency hearing in inbred CD-1 mice. The p.Ala88Val (A88V) mutation in the gene coding for the gap-junction protein connexin30 (Cx30) protects the cochlear basal turn of adult CD-1Cx30(A88V/A88V) mice from degeneration and rescues hearing. Here we report that the passive compliance of the cochlear partition and active frequency tuning of the basilar membrane are enhanced in the cochleae of CD-1Cx30(A88V/A88V) compared to CBA/J mice with sensitive high-frequency hearing, suggesting that gap junctions contribute to passive cochlear mechanics and energy distribution in the active cochlea. Surprisingly, the endocochlear potential that drives mechanoelectrical transduction currents in outer hair cells and hence cochlear amplification is greatly reduced in CD-1Cx30(A88V/A88V) mice. Yet, the saturating amplitudes of cochlear microphonic potentials in CD-1Cx30(A88V/A88V) and CBA/J mice are comparable. Although not conclusive, these results are compatible with the proposal that transmembrane potentials, determined mainly by extracellular potentials, drive somatic electromotility of outer hair cells."],["dc.description.sponsorship","Medical Research Council; German Research Foundation (DFG) [1608]"],["dc.identifier.doi","10.1038/ncomms14530"],["dc.identifier.isi","000394499600001"],["dc.identifier.pmid","28220769"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14387"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43215"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.haserratum","/handle/2/69159"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.lastpage","1"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Chapochnikov, Nikolai M."],["dc.contributor.author","Frank, Thomas"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Neef, Andreas"],["dc.contributor.author","Khimich, Darina"],["dc.contributor.author","Egner, Alexander"],["dc.contributor.author","Wolf, Fred"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2011-04-12T13:30:30Z"],["dc.date.accessioned","2021-10-11T11:34:47Z"],["dc.date.available","2011-04-12T13:30:30Z"],["dc.date.available","2021-10-11T11:34:47Z"],["dc.date.issued","2009"],["dc.identifier.citation","Chapochnikov, Nikolai M; Frank, Thomas; Strenzke, Nicola; Neef, Andreas; Khimich, Darina; Egner, Alexander; Wolf, Fred; Moser, Tobias (2009): Modeling the origin of functional heterogeneity among auditory nerve fibers - BMC Neuroscience, Vol. 10, Nr. Suppl 1, p. P220-"],["dc.identifier.doi","10.1186/1471-2202-10-S1-P220"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90701"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Fakultät für Physik"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","http://goedoc.uni-goettingen.de/licenses"],["dc.subject","heterogeneity; auditory nerve fibers"],["dc.subject.ddc","530"],["dc.subject.ddc","573"],["dc.subject.ddc","573.8"],["dc.subject.ddc","612"],["dc.subject.ddc","612.8"],["dc.title","Modeling the origin of functional heterogeneity among auditory nerve fibers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]