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dc.creatorRamírez Latorre, José 
dc.date.accessioned2014-08-13T19:00:17Z
dc.date.available2014-08-13T19:00:17Z
dc.date.created2012-12-20
dc.date.issued2012 
dc.identifier.issnISSN:1932-6203
dc.identifier.urihttp://repository.urosario.edu.co/handle/10336/8838
dc.description.abstractMany connections in the basal ganglia are made around birth when animals are exposed to a host of new affective, cognitive, and sensori-motor stimuli. It is thought that dopamine modulates cortico-striatal synapses that result in the strengthening of those connections that lead to desired outcomes. We propose that there must be a time before which stimuli cannot be processed into functional connections, otherwise it would imply an effective link between stimulus, response, and reward in uterus. Consistent with these ideas, we present evidence that early in development dopamine neurons are electrically immature and do not produce high-frequency firing in response to salient stimuli. We ask first, what makes dopamine neurons immature? and second, what are the implications of this immaturity for the basal ganglia? As an answer to the first question, we find that at birth the outward current is small (3nS-V), insensitive to Ca2+, TEA, BK, and SK blockers. Rapidly after birth, the outward current increases to 15nS-V and becomes sensitive to Ca2+, TEA, BK, and SK blockers. We make a detailed analysis of the kinetics of the components of the outward currents and produce a model for BK and SK channels that we use to reproduce the outward current, and to infer the geometrical arrangement of BK and Ca2+ channels in clusters. In the first cluster, T-type Ca2+ and BK channels are coupled within distances of similar to 20 nm (200 parallel to). The second cluster consists of L-type Ca2+ and BK channels that are spread over distances of at least 60 nm. As for the second question, we propose that early in development, the mechanism of action selection is in a "locked-in" state that would prevent dopamine neurons from reinforcing cortico-striatal synapses that do not have a functional experiential-based value.
dc.format.mediumRecurso electrónico
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofPLOS ONE ISSN: 1932-6203 V. 7 N. 12 Dic 20, 2012
dc.relation.urihttp://apps.webofknowledge.com.ez.urosario.edu.co/full_record.do?product=UA&search_mode=GeneralSearch&qid=5&SID=2FeAM82FH4kCimTQW7c&page=1&doc=1
dc.sourcereponame:Repositorio Institucional EdocUR
dc.sourceinstname:Universidad del Rosario
dc.subject.ddcFisiología humana 
dc.titleFunctional Upregulation of Ca2+ -Activated K+ Channels in the Development of Substantia Nigra Dopamine Neurons
dc.typearticle
dc.audienceComunidad Rosarista
dc.publisherUniversidad del Rosario
dc.subject.keywordPARS COMPACTA NEURONS
dc.subject.keywordBASAL GANGLIA
dc.subject.keywordPOTASSIUM CHANNELS
dc.subject.keywordCALCIUM-CHANNELS
dc.subject.keywordHIGH-FREQUENCY
dc.subject.keywordBK CHANNELS
dc.subject.keywordBK CHANNELS
dc.subject.keywordIN-VITRO
dc.subject.keywordIN-VITRO
dc.subject.keywordPARASYMPATHETIC NEURONS
dc.subject.keywordPOSTNATAL-DEVELOPMENT
dc.subject.keywordNEONATAL-RATS
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.subject.decsDopamina
dc.subject.decsNeuronas
dc.subject.decsSinapsis
dc.subject.decsNeurología
dc.subject.decsBioquímica
dc.type.spaArtículo
dc.rights.accesoAbierto (Texto completo)
dc.type.hasVersioninfo:eu-repo/semantics/acceptedVersion
dc.format.tipoDocumento
dc.rights.licenciaEL AUTOR, manifiesta que la obra objeto de la presente autorización es original y la realizó sin violar o usurpar derechos de autor de terceros, por lo tanto la obra es de exclusiva autoría y tiene la titularidad sobre la misma.
dc.creator.googleRamírez Latorre, José A.


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