Transplantation of inhibitory precursor cells from medial ganglionic eminence produces distinct responses in two different models of acute seizure induction

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dc.citation.volume70
dc.contributor.authorPaiva, Daisylea de Souza [UNIFESP]
dc.contributor.authorAlves Romariz, Simone Amaro [UNIFESP]
dc.contributor.authorValente, Maria Fernanda [UNIFESP]
dc.contributor.authorMoraes, Luiz Bruno [UNIFESP]
dc.contributor.authorCovolan, Luciene [UNIFESP]
dc.contributor.authorCalcagnotto, Maria Elisa
dc.contributor.authorLongo, Beatriz Monteiro [UNIFESP]
dc.coverageSan Diego
dc.date.accessioned2020-07-13T11:53:21Z
dc.date.available2020-07-13T11:53:21Z
dc.date.issued2017
dc.description.abstractMedial ganglionic eminence (MGE) is one of the sources of inhibitory interneurons during development. Following transplantation in postnatal developing brain, MGE cells can increase local inhibition suggesting a possible protection to GABAergic dysfunction in brain disorders, such as epilepsy. Since it has been shown that MGE-derived cells harvested as neurospheres are able to suppress seizures, it might be important to investigate whether these protective effects would change in different seizure models. Here, we used pentylenetetrazole(PTZ) and maximal electroshock (MES)-induced seizure models to test whether the transplantation of MGE cells would increase the threshold to trigger acute seizures. When transplanted into the neocortex (layers 3-4) of neonatal mice (postnatal days 3-4), MGE cells were able to survive and were mainly found in piriform cortex, fimbria, and ventricular wall regions. Additionally, the number of GFP + cells found in the brains of mice induced with PTZ and MES differed significantly and suggests proliferation and larger survival rate of MGE-transplanted cells after PTZ, but not MES-induced seizures. Following transplantation, there was a reduction in the number of animals presenting mild and severe seizures induced by PTZ. Furthermore, MGE-cell transplantation was able to increase threshold to seizures induced by PTZ, but was not able to prevent seizure spread induced by MES. (C) 2017 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniv Fed Sao Paulo UNIFESP, Lab Neurofisiol, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Rio Grande do Sul, Porto Alegre, RS, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo UNIFESP, Lab Neurofisiol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCNPq
dc.format.extent125-130
dc.identifierhttp://dx.doi.org/10.1016/j.yebeh.2017.03.015
dc.identifier.citationEpilepsy & Behavior. San Diego, v. 70, p. 125-130, 2017.
dc.identifier.doi10.1016/j.yebeh.2017.03.015
dc.identifier.issn1525-5050
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/54560
dc.identifier.wosWOS:000402447700020
dc.language.isoeng
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofEpilepsy & Behavior
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPentylenetetrazoleen
dc.subjectMaximal electroshocken
dc.subjectNeurosphereen
dc.subjectMedial ganglionic eminenceen
dc.subjectAcute seizureen
dc.titleTransplantation of inhibitory precursor cells from medial ganglionic eminence produces distinct responses in two different models of acute seizure inductionen
dc.typeinfo:eu-repo/semantics/article
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