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  3. FCEN - Facultad de Ciencias Exactas y Naturales. UBA
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Campo DC Valor Lengua/Idioma
dc.provenanceFacultad de Ciencias Exactas y Naturales de la UBA-
dc.contributorDe San Martín, J.Z.-
dc.contributorPyott, S.-
dc.contributor<div class="autor_fcen" id="559">Ballestero, J.</div>-
dc.contributor<div class="autor_fcen" id="4549">Katz, E.</div>-
dc.creatorDe San Martín, J.Z.-
dc.creatorPyott, S.-
dc.creator<div class="autor_fcen" id="559">Ballestero, J.</div>-
dc.creator<div class="autor_fcen" id="4549">Katz, E.</div>-
dc.date.accessioned2018-05-04T21:57:28Z-
dc.date.accessioned2018-05-28T15:48:28Z-
dc.date.available2018-05-04T21:57:28Z-
dc.date.available2018-05-28T15:48:28Z-
dc.date.issued2010-
dc.identifier.urihttp://10.0.0.11:8080/jspui/handle/bnmm/68493-
dc.descriptionIn the mammalian auditory system, the synapse between efferent olivocochlear (OC) neurons and sensory cochlear hair cells is cholinergic, fast, and inhibitory. This efferent synapse is mediated by the nicotinic α9α10 receptor coupled to the activation of SK2 Ca 2+-activated K+ channels that hyperpolarize the cell. So far, the ion channels that support and/or modulate neurotransmitter release from the OC terminals remain unknown. To identify these channels, we used an isolated mouse cochlear preparation and monitored transmitter release from the efferent synaptic terminals in inner hair cells (IHCs) voltage clamped in the whole-cell recording configuration. Acetylcholine (ACh) release was evoked by electrically stimulating the efferent fibers that make axosomatic contacts with IHCs before the onset of hearing. Using the specific antagonists for P/Q- and N-type voltage-gated calcium channels (VGCCs), ω-agatoxin IVA and ω-conotoxin GVIA, respectively, we show that Ca2+ entering through both types of VGCCs support the release process at this synapse. Interestingly, we found that Ca2+ entering through the dihydropiridine-sensitive L-type VGCCs exerts a negative control on transmitter release. Moreover, using immunostaining techniques combined with electrophysiology and pharmacology, we show that BK Ca2+-activated K+ channels are transiently expressed at the OC efferent terminals contacting IHCs and that their activity modulates the release process at this synapse. The effects of dihydropiridines combined with iberiotoxin, a specific BK channel antagonist, strongly suggest that L-type VGCCs negatively regulate the release of ACh by fueling BK channels that are known to curtail the duration of the terminal action potential in several types of neurons. Copyright © 2010 the authors.-
dc.descriptionFil:Ballestero, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Katz, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.formatapplication/pdf-
dc.languageeng-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttp://creativecommons.org/licenses/by/2.5/ar-
dc.sourceJ. Neurosci. 2010;30(36):12157-12167-
dc.source.urihttp://digital.bl.fcen.uba.ar/Download/paper/paper_02706474_v30_n36_p12157_DeSanMartin.pdf-
dc.subjectacetylcholine-
dc.subjectcalcium activated potassium channel-
dc.subjectcalcium channel L type-
dc.subjectcalcium channel N type-
dc.subjectcalcium channel P type-
dc.subjectcalcium channel Q type-
dc.subjectcalcium ion-
dc.subjectcalretinin-
dc.subjectcell marker-
dc.subjectiberiotoxin-
dc.subjectnifedipine-
dc.subjectnitrendipine-
dc.subjectomega agatoxin IVA-
dc.subjectomega conotoxin GVIA-
dc.subjectsynapsin-
dc.subjectvoltage gated calcium channel-
dc.subjectacetylcholine release-
dc.subjectanimal cell-
dc.subjectanimal tissue-
dc.subjectarticle-
dc.subjectcochlear nerve-
dc.subjectcontrolled study-
dc.subjectCorti organ-
dc.subjectefferent nerve-
dc.subjectelectrostimulation-
dc.subjectfemale-
dc.subjectfluorescence microscopy-
dc.subjecthair cell-
dc.subjectimmunohistochemistry-
dc.subjectinhibitory postsynaptic potential-
dc.subjectisolated organ-
dc.subjectmale-
dc.subjectmouse-
dc.subjectnonhuman-
dc.subjectpharmacological blocking-
dc.subjectpriority journal-
dc.subjectprotein expression-
dc.subjectprotein function-
dc.subjectprotein localization-
dc.subjectsynapse-
dc.subjectvoltage clamp-
dc.subjectwhole cell-
dc.subjectAcetylcholine-
dc.subjectAnimals-
dc.subjectAnimals, Newborn-
dc.subjectBiophysics-
dc.subjectCalcium-
dc.subjectCalcium Channel Blockers-
dc.subjectDose-Response Relationship, Drug-
dc.subjectElectric Stimulation-
dc.subjectFemale-
dc.subjectHair Cells, Auditory, Inner-
dc.subjectInhibitory Postsynaptic Potentials-
dc.subjectMale-
dc.subjectMice-
dc.subjectMice, Inbred BALB C-
dc.subjectOlivary Nucleus-
dc.subjectOrgan of Corti-
dc.subjectPatch-Clamp Techniques-
dc.subjectPeptides-
dc.subjectPotassium Channel Blockers-
dc.subjectPotassium Channels, Calcium-Activated-
dc.subjectSynapses-
dc.subjectSynaptic Transmission-
dc.titleCa2+and Ca2+-activated K+ channels that support and modulate transmitter release at the olivocochlear efferent-inner hair cell synapse-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:ar-repo/semantics/artículo-
dc.typeinfo:eu-repo/semantics/publishedVersion-
Aparece en las colecciones: FCEN - Facultad de Ciencias Exactas y Naturales. UBA

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