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dc.contributor.author
Gan, Lu
dc.contributor.author
Falzone, Tomas Luis
dc.contributor.author
Zhang, Kehong
dc.contributor.author
Rubinstein, Marcelo
dc.contributor.author
Baldessarini, Ross J.
dc.contributor.author
Tarazi, Frank I.
dc.date.available
2019-07-18T18:02:59Z
dc.date.issued
2004-03
dc.identifier.citation
Gan, Lu; Falzone, Tomas Luis; Zhang, Kehong; Rubinstein, Marcelo; Baldessarini, Ross J.; et al.; Enhanced expression of dopamine D1 and glutamate NMDA receptors in dopamine D4 receptor knockout mice; Springer; Journal Of Molecular Neuroscience : Mn.; 22; 3; 3-2004; 167-177
dc.identifier.issn
0895-8696
dc.identifier.uri
http://hdl.handle.net/11336/79811
dc.description.abstract
Expression of dopamine ([DA] D1 and D2) and glutamate ([Glu], (N-methyl-D-aspartic acid [NMDA], α-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid [AMPA], and kanaic acid [KA]) receptor types were analyzed autoradiographically in forebrain regions of D4 receptor knockout mice and their wild-type controls. Selective radioligand binding to D4 receptors was virtually absent in D4 receptor knockout mouse brain in contrast to significant specific D4 binding in forebrain tissue of wild-type controls. Labeling of D1 receptors was significantly increased in nucleus accumbens (NAc; 39%) and caudate putamen (CPu; 42%) of D4-knockout mice vs wild-type controls. In addition, NMDA receptor labeling was significantly increased in NAc (31%), CPu (40%), and hippocampal CA1 (21%) and CA3 (25%) regions of D 4 knockouts vs wild-type controls. No changes in D2, AMPA or KA receptors were found. The findings suggest that D1, D 4, and NMDA receptors might interact functionally and that developmental absence of D4 receptors might trigger compensatory mechanisms that enhance expression of D1 receptors in NAc and CPu, and NMDA receptors in NAc, CPu, and hippocampus. The findings also encourage cautious interpretation of results in knockout mice with targeted absence of specific genes, as complex adaptive changes not directly related to the missing gene might contribute to physiological and behavioral responses.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Autoradiography
dc.subject
Caudate Putamen
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D4-Receptor
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Dopamine Receptors
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Genetic Knockout
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Glutamate Receptors
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Mutant Mice
dc.subject.classification
Neurociencias
dc.subject.classification
Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Enhanced expression of dopamine D1 and glutamate NMDA receptors in dopamine D4 receptor knockout mice
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-07-16T14:14:20Z
dc.journal.volume
22
dc.journal.number
3
dc.journal.pagination
167-177
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Oregon
dc.description.fil
Fil: Gan, Lu. McLean Division of Massachusetts General Hospital; Estados Unidos. Harvard Medical School; Estados Unidos
dc.description.fil
Fil: Falzone, Tomas Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
dc.description.fil
Fil: Zhang, Kehong. McLean Division of Massachusetts General Hospital; Estados Unidos. Harvard Medical School; Estados Unidos
dc.description.fil
Fil: Rubinstein, Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
dc.description.fil
Fil: Baldessarini, Ross J.. McLean Division of Massachusetts General Hospital; Estados Unidos. Harvard Medical School; Estados Unidos
dc.description.fil
Fil: Tarazi, Frank I.. McLean Division of Massachusetts General Hospital; Estados Unidos. Harvard Medical School; Estados Unidos
dc.journal.title
Journal Of Molecular Neuroscience : Mn.
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pubmed/14997010
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1385/JMN:22:3:167
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1385%2FJMN%3A22%3A3%3A167
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