SUMMARYMost of the c-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.
The GABAergic system is critically involved in the modulation of anxiety levels, and dysfunction of GABAergic neurotransmission appears to be involved in the development of generalized anxiety disorder. Precursor cells from the medial ganglionic eminence (MGE) have the ability to migrate and differentiate into inhibitory GABAergic interneurons after being transplanted into the mouse brain. Thus, transplantation of interneuronal precursor cells derived from the MGE into a postnatal brain could modify the neuronal circuitry, increasing GABAergic tone and decreasing anxiety-like behavior in animals. Our aim was to verify the in vivo effects of transplanted MGE cells by evaluating anxiety-like behavior in mice. MGE cells from 14-day green fluorescent protein (GFP) embryos were transplanted into newborn mice. At 15, 30, and 60 days posttransplant, the animals were tested for anxiety behavior with the elevated plus maze (EPM) test. Our results show that transplanted cells from MGE were able to migrate to different regions of the brain parenchyma and to differentiate into inhibitory interneurons. The neuronal precursor cell transplanted animals had decreased levels of anxiety, indicating a specific function of these cells in vivo. We suggested that transplantation of MGE-derived neuronal precursors into neonate brain could strengthen the inhibitory function of the GABAergic neuronal circuitry related to anxiety-like behavior in mice.
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