Mostrar el registro sencillo del ítem

dc.contributor.author
Shabel, Steven J.  
dc.contributor.author
Proulx, Christophe D.  
dc.contributor.author
Piriz, Joaquin  
dc.contributor.author
Malinow, Roberto  
dc.date.available
2017-05-08T22:09:01Z  
dc.date.issued
2014-09  
dc.identifier.citation
Shabel, Steven J.; Proulx, Christophe D.; Piriz, Joaquin; Malinow, Roberto; GABA/glutamate co-release controls habenula output and is modified by antidepressant treatment; American Association for the Advancement of Science; Science; 345; 6203; 9-2014; 1494-1498  
dc.identifier.issn
0036-8075  
dc.identifier.uri
http://hdl.handle.net/11336/16125  
dc.description.abstract
The lateral habenula (LHb), a key regulator of monoaminergic brain regions, is activated by negatively valenced events. Its hyperactivity is associated with depression. Although enhanced excitatory input to the LHb has been linked to depression, little is known about inhibitory transmission. We discovered that γ-aminobutyric acid (GABA) is co-released with its functional opponent, glutamate, from long-range basal ganglia inputs (which signal negative events) to limit LHb activity in rodents. At this synapse, the balance of GABA/glutamate signaling is shifted toward reduced GABA in a model of depression and increased GABA by antidepressant treatment. GABA and glutamate co-release therefore controls LHb activity, and regulation of this form of transmission may be important for determining the effect of negative life events on mood and behavior.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
American Association for the Advancement of Science  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Lateral Habenula  
dc.subject
Depression  
dc.subject
Co-Release  
dc.subject.classification
Neurociencias  
dc.subject.classification
Medicina Básica  
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
GABA/glutamate co-release controls habenula output and is modified by antidepressant treatment  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2017-04-26T14:13:56Z  
dc.journal.volume
345  
dc.journal.number
6203  
dc.journal.pagination
1494-1498  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Washington D. C.  
dc.description.fil
Fil: Shabel, Steven J.. University of California at San Diego; Estados Unidos  
dc.description.fil
Fil: Proulx, Christophe D.. University of California at San Diego; Estados Unidos  
dc.description.fil
Fil: Piriz, Joaquin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina  
dc.description.fil
Fil: Malinow, Roberto. University of California at San Diego; Estados Unidos  
dc.journal.title
Science  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1126/science.1250469  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://science.sciencemag.org/content/345/6203/1494  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305433/