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Updated: May 21, 2025

Viral-mediated Labeling and Transplantation of Medial Ganglionic Eminence MGE Cells for In Vivo Studies
Published on: April 23, 2015
Medial ganglionic eminence transplantation restores inhibition after central visual system brain injury
Bowen Hou1,2, Jisu Eom1,2, David C Lyon1,2,3
1Department of Anatomy & Neurobiology, UCI School of Medicine, Med. Sci. B, Room 240, Irvine, CA 92697, USA.
Inhibitory interneurons are critical regulators of visual circuit function and plasticity, but they are partially lost after brain injury. It has been hypothesized that embryonic medial ganglionic eminence (MGE) progenitors transplanted into visual cortex may facilitate brain repair, but there is no evidence that MGE cells modify inhibition in the damaged visual system. Here, we demonstrate that MGE progenitors transplanted into primary visual cortex of adult mice with traumatic brain injury (TBI) migrate widely throughout the lesioned area and express molecular markers of mature inhibitory interneurons. Whole-cell voltage-clamp recordings of inhibitory postsynaptic currents obtained from layer 2/3 host neurons, 45-60 days after transplantation, revealed a significant loss of GABA-mediated synaptic inhibition after TBI. Following MGE transplantation, we found significant increases in synaptic inhibition in regions of visual cortex containing transplanted MGE progenitors. Our results therefore provide direct evidence that MGE transplantation enhances local inhibition after central visual system brain injury.
Inhibitory interneurons are critical regulators of visual circuit function and plasticity, but they are partially lost after brain injury. It has been hypothesized that embryonic medial ganglionic eminence (MGE) progenitors transplanted into visual cortex may facilitate brain repair, but there is no evidence that MGE cells modify inhibition in the damaged visual system. Here, we demonstrate that MGE progenitors transplanted into primary visual cortex of adult mice with traumatic brain injury (TBI) migrate widely throughout the lesioned area and express molecular markers of mature inhibitory interneurons. Whole-cell voltage-clamp recordings of inhibitory postsynaptic currents obtained from layer 2/3 host neurons, 45-60 days after transplantation, revealed a significant loss of GABA-mediated synaptic inhibition after TBI. Following MGE transplantation, we found significant increases in synaptic inhibition in regions of visual cortex containing transplanted MGE progenitors. Our results therefore provide direct evidence that MGE transplantation enhances local inhibition after central visual system brain injury.
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