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Effect of neuronal precursor cells derived from medial ganglionic eminence in an acute epileptic seizure model
Author(s) -
Calcagnotto Maria E.,
Ruiz Lorena P.,
Blanco Miriam M.,
SantosJunior Jair G.,
Valente Maria F.,
Patti Camila,
FrussaFilho Roberto,
Santiago Marcelo F.,
Zipancic Ivan,
ÁlvarezDolado Manuel,
Mello Luiz E.,
Longo Beatriz M.
Publication year - 2010
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2010.02614.x
Subject(s) - ganglionic eminence , neuroscience , gabaergic , inhibitory postsynaptic potential , epilepsy , biology , hippocampal formation , cerebrum , central nervous system
Summary Most of the γ‐aminobutyric acid (GABA)ergic interneurons in the cerebral cortex originate from restricted regions of the ventral telencephalon known as the caudal and medial ganglionic eminence (MGE) and from the preoptic area. It is well established that dysfunction of GABAergic interneurons can lead to epilepsy. During the last decade new approaches to prevent, reduce, or reverse the epileptic condition have been studied, including cell‐based therapy from different sources. Recent studies have shown that transplanted neuronal precursor cells derived from MGE have the ability to migrate, differentiate into inhibitory GABAergic interneurons, and integrate into cortical and hippocampal networks, modifying the inhibitory tone in the host brain. Therefore, transplantation of neuronal precursors derived from MGE into the postnatal central nervous system (CNS) could modify the neuronal circuitry in neurologic diseases in which inhibitory synaptic function is altered, such as in epilepsy. Here, we evaluated the seizure susceptibility of mice transplanted with MGE‐derived cells in the maximum electroconvulsive shock (MES) model and we review some data from different studies using GABAergic precursor or GABA‐releasing cell grafts in animal models of seizure and epilepsy.