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Updated: Nov 18, 2025

Homochronic Transplantation of Interneuron Precursors into Early Postnatal Mouse Brains
Published on: June 8, 2018
Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex
XiaoTing Zheng1, Kirstie J Salinas1, Dario X Figueroa Velez1
1Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA, 92697-2715, USA.
Transplanted embryonic interneurons restore adult brain plasticity by rejuvenating host parvalbumin (PV) interneurons. This process relies on Neuregulin (NRG1)/ErbB4 signaling in host PV cells, not donor cells.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Cortical Plasticity
Background:
- Adult brains exhibit reduced sensitivity to environmental changes compared to juvenile brains.
- Embryonic interneuron transplantation can restore plasticity in the adult visual cortex.
- The precise mechanism of transplant-induced plasticity (direct vs. indirect) remains unclear.
Purpose of the Study:
- To determine if transplanted interneurons directly mediate plasticity or indirectly modify host circuitry.
- To investigate the role of Neuregulin (NRG1)/ErbB4 signaling in transplant-induced cortical plasticity.
Main Methods:
- Utilized mouse models with transplanted embryonic interneurons into the adult visual cortex.
- Examined the effects of visual deprivation on host and transplanted parvalbumin (PV) interneurons.
- Manipulated Neuregulin (NRG1)/ErbB4 signaling in host and donor PV interneurons.
- Assessed cortical plasticity through circuit reorganization and visual response changes.
Main Results:
- Transplant-induced circuit reorganization is mediated by NRG1/ErbB4 signaling specifically in host PV interneurons.
- Visual deprivation reduces host PV interneuron activity, but not transplanted PV interneuron activity.
- Exogenous NRG1 prevents activity reduction and blocks transplant-induced plasticity.
- Deleting ErbB4 from host PV interneurons abolishes plasticity; deleting from donor PV interneurons has no effect.
Conclusions:
- Transplanted interneurons reactivate cortical plasticity by rejuvenating host PV interneuron function.
- NRG1/ErbB4 signaling in host PV interneurons is essential for restoring plasticity after interneuron transplantation.
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