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Epilepsy Behav ; 70(Pt A): 125-130, 2017 05.
Article in English | MEDLINE | ID: mdl-28427019

ABSTRACT

Medial 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.


Subject(s)
Disease Models, Animal , Electroshock/adverse effects , Median Eminence/transplantation , Neural Stem Cells/transplantation , Pentylenetetrazole/toxicity , Seizures/therapy , Acute Disease , Animals , Female , Hippocampus/physiopathology , Interneurons , Male , Median Eminence/cytology , Mice , Mice, Inbred C57BL , Mice, Transgenic , Neocortex/physiopathology , Pregnancy , Seizures/etiology , Seizures/physiopathology
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