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dc.contributor.authorWang, Leen_US
dc.contributor.authorColburn, H. Stevenen_US
dc.coverage.spatialUnited Statesen_US
dc.date2011-10-25
dc.date.accessioned2018-05-31T14:25:20Z
dc.date.available2018-05-31T14:25:20Z
dc.date.issued2012-04
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/22160752
dc.identifier.citationLe Wang, H Steven Colburn. 2012. "A modeling study of the responses of the lateral superior olive to ipsilateral sinusoidally amplitude-modulated tones.." J Assoc Res Otolaryngol, v. 13, issue 2, pp. 249 - 267.
dc.identifier.issn1438-7573
dc.identifier.urihttps://hdl.handle.net/2144/29228
dc.description.abstractThe lateral superior olive (LSO) is a brainstem nucleus that is classically understood to encode binaural information in high-frequency sounds. Previous studies have shown that LSO cells are sensitive to envelope interaural time difference in sinusoidally amplitude-modulated (SAM) tones (Joris and Yin, J Neurophysiol 73:1043-1062, 1995; Joris, J Neurophysiol 76:2137-2156, 1996) and that a subpopulation of LSO neurons exhibit low-threshold potassium currents mediated by Kv1 channels (Barnes-Davies et al., Eur J Neurosci 19:325-333, 2004). It has also been shown that in many LSO cells the average response rate to ipsilateral SAM tones decreases with modulation frequency above a few hundred Hertz (Joris and Yin, J Neurophysiol 79:253-269, 1998). This low-pass feature is not directly inherited from the inputs to the LSO since the response rate of these input neurons changes little with increasing modulation frequency. In the current study, an LSO cell model is developed to investigate mechanisms consistent with the responses described above, notably the emergent rate decrease with increasing frequency. The mechanisms explored included the effects of after-hyperpolarization (AHP) channels, the dynamics of low-threshold potassium channels (KLT), and the effects of background inhibition. In the model, AHP channels alone were not sufficient to induce the observed rate decrease at high modulation frequencies. The model also suggests that the background inhibition alone, possibly from the medial nucleus of the trapezoid body, can account for the small rate decrease seen in some LSO neurons, but could not explain the large rate decrease seen in other LSO neurons at high modulation frequencies. In contrast, both the small and large rate decreases were replicated when KLT channels were included in the LSO neuron model. These results support the conclusion that KLT channels may play a major role in the large rate decreases seen in some units and that background inhibition may be a contributing factor, a factor that could be adequate for small decreases.en_US
dc.description.sponsorshipR01 DC000100 - NIDCD NIH HHS; DC00100 - NIDCD NIH HHSen_US
dc.format.extentp. 249 - 267en_US
dc.languageeng
dc.relation.ispartofJ Assoc Res Otolaryngol
dc.subjectNeurosciencesen_US
dc.subjectLSOen_US
dc.subjectCATen_US
dc.subjectHumansen_US
dc.subjectOtorhinolaryngologyen_US
dc.subjectScience & technologyen_US
dc.subjectLife sciences & biomedicineen_US
dc.subjectNeurosciences & neurologyen_US
dc.subjectLow-threshold potassium channelen_US
dc.subjectAuditory brainstemen_US
dc.subjectCochlear nucleus bushy cellsen_US
dc.subjectEnvelope processingen_US
dc.subjectVentral cochlear nucleusen_US
dc.subjectUnit excitatory responsesen_US
dc.subjectAuditory-nerve fibersen_US
dc.subjectLow-frequency neuronsen_US
dc.subjectBushy cell axonsen_US
dc.subjectSound localizationen_US
dc.subjectPotassium currentsen_US
dc.subjectTonal stimulien_US
dc.subjectS segmenten_US
dc.subjectAcoustic stimulationen_US
dc.subjectCochlear nerveen_US
dc.subjectComputer simulationen_US
dc.subjectMembrane potentialsen_US
dc.subjectModels, biologicalen_US
dc.subjectOlivary nucleusen_US
dc.subjectPotassium channelsen_US
dc.subjectClinical sciencesen_US
dc.titleA modeling study of the responses of the lateral superior olive to ipsilateral sinusoidally amplitude-modulated tonesen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s10162-011-0300-5
pubs.elements-sourcepubmeden_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Engineeringen_US
pubs.organisational-groupBoston University, College of Engineering, Department of Biomedical Engineeringen_US
pubs.publication-statusPublisheden_US


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