Transplanted cells are essential for the induction but not the expression of cortical plasticity

Abstract

Transplantation of even a small number of embryonic inhibitory neurons from the medial ganglionic eminence (MGE) into postnatal visual cortex makes it lose responsiveness to an eye deprived of vision when the transplanted neurons reach the age of the normal critical period of activity-dependent ocular dominance (OD) plasticity. The transplant might induce OD plasticity in the host circuitry or might instead construct a parallel circuit of its own to suppress cortical responses to the deprived-eye. We transplanted MGE neurons expressing archaerhodopsin, closed one eyelid for 4-5 days, and, as expected, observed transplant-induced OD plasticity. This plasticity was evident even when the activity of the transplanted cells was suppressed optogenetically, demonstrating that the plasticity was produced by changes in the host visual cortex.

Interneuron transplantation: a prospective surgical therapy for medically refractory epilepsy

“…42 Additionally, transplant populations may be engineered to deliver trophic or neuroprotective agents. They may also be designed to express light-or chemically sensitive ion channels or transporters, allowing for optogenetic 9,24,27 and chemogenetic 64 control of transplant activity. Finally, donor populations may also be engineered to express inducible cytotoxins, allowing the ablation of transplanted cells.…”