Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/67844
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dc.contributor.authorGonzalez-Burgos, I.
dc.contributor.authorVelazquez-Zamora, D.A.
dc.contributor.authorBeas-Zárate, Carlos
dc.date.accessioned2015-11-19T18:52:32Z-
dc.date.available2015-11-19T18:52:32Z-
dc.date.issued2009
dc.identifier.urihttp://hdl.handle.net/20.500.12104/67844-
dc.description.abstractHippocampal vulnerability to excitotoxicity has been widely studied along with its implication to learning and memory. Neonatal glutamate excitotoxicity induces loss of CA1 pyramidal neurons in adult rats concomitantly with some plastic changes in the dendritic spines of surviving neurons. At least in part, these may underlie the place learning impairments seen in previous studies based on a similar excitotoxicity-inducing model. In the present study, cytoarchitecture of dentate gyrus, CA3 and CA1 fields were evaluated in 120-day-old rats, after they had been neonatally treated with glutamate as monosodium salt. Dentate granule cells and CA1 pyramidal neurons were less than those counted in NaCl-treated control animals. In addition, dentate granule cells had more dendrites as well as more branched spines. Spine density in CA1 pyramidal neurons was greater than in the controls. Additionally, thin and mushroom spines were proportionally more abundant in monosodium glutamate-treated animals. No effects were seen in the hippocampal CA3 field. Our results strongly suggest a long-term induction of plastic changes in the cytoarchitecture of the hippocampal trisynaptic circuit neurons after cell death provoked by the monosodium glutamate-induced excitotoxicity. These plastic events as well as the aberrant expression of the glutamate NMDA receptors resulting from monosodium glutamate neonatal treatment could be strongly associated with the place learning impairments previously reported. © 2009 ISDN.
dc.titleDamage and plasticity in adult rat hippocampal trisynaptic circuit neurons after neonatal exposure to glutamate excitotoxicity
dc.typeArticle
dc.identifier.doi10.1016/j.ijdevneu.2009.08.016
dc.relation.ispartofjournalInternational Journal of Developmental Neuroscience
dc.relation.ispartofvolume27
dc.relation.ispartofissue8
dc.relation.ispartofpage741
dc.relation.ispartofpage745
dc.subject.keywordDendritic spines; Excitotoxicity; Glutamate; Hippocampus; Trisynaptic circuit
dc.contributor.affiliationGonzález-Burgos, I., Laboratorio de Psicobiología, División de Neurociencias, Centro de Investigación Biomédica de Occidente, Guadalajara, Mexico, Depto. de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Jal., Mexico; Velázquez-Zamora, D.A., Laboratorio de Psicobiología, División de Neurociencias, Centro de Investigación Biomédica de Occidente, Guadalajara, Mexico; Beas-Zárate, C., Laboratorio de Neurobiología Celular y Molecular, División de Neurociencias, Centro de Investigación Biomédica de Occidente, Guadalajara, Mexico, Depto. de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Jal., Mexico
dc.contributor.affiliationBeas-Zárate, Carlos., Universidad de Guadalajara. Centro Universitario de Ciencias Biológicas y Agropecuarias
dc.relation.isReferencedByScopus
dc.relation.isReferencedByWOS
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-70449523696&partnerID=40&md5=1f0bdd7db89e70c0295f24c72df67f72
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