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 either archaerhodopsin or channelrhodopsin into the visual cortex of both male and female mice, closed one eyelid for 4-5 d, and, as expected, observed transplant-induced OD plasticity. This plasticity was evident even when the activity of the transplanted cells was suppressed or enhanced optogenetically, demonstrating that the plasticity was produced by changes in the host visual cortex.

Host interneurons mediate plasticity reactivated by embryonic inhibitory cell transplantation in mouse visual cortex

“…3b, c). Consistent with a previous study 23 , once integrated into the host circuit, the transplanted interneurons may not directly contribute to the expression of ODP of the recipients.…”

“…As the transplanted VGAT −/− interneurons in that study did not fully mature, reflected in their abnormally developed axonal and dendritic processes, release of the necessary factors for the rejuvenation of NRG1/ ErbB4 signaling in the host PV interneurons may have been prevented. In support of our conclusion, another recent transplantation study shows that suppressing the activity of transplanted interneurons using optogenetics after MD does not prevent the expression of transplant-induced ODP 23 . We confirmed this result by selectively suppressing the activity in the transplanted PV cells during MD using DREADD-based chemogenetic approach ( Supplementary Fig.…”

Gamma rhythms and visual information in mouse V1 specifically modulated by somatostatin+ neurons in reticular thalamus

“…Given that we used saturating illumination to activate these neurons, the activation of SST-nRT input to dLGN was likely uniform rather than focal. Thereafter, extracellular recordings of single unit activity and LFPs were made using a double-shank 128-channel microelectrode array placed in the V1 of mice that were free to stand or run on a polystyrene ball floating on an air stream (Figure 2A) (Du et al, 2011;Hoseini et al, 2019). Mice viewed a gray blank screen while a blue light (473 nm, ~63 mW/mm 2 ) was delivered using an optical fiber implanted above nRT during different locomotion states (Figure 2B).…”

Stability in the Face of Change: Lifelong Experience-Dependent Plasticity in the Sensory Cortex

“…The host cortex becomes responsive to monocular deprivation once transplanted interneurons reach the critical period age, indicating that additional intrinsic regulators of interneuron maturation and critical period timing exist. More recent work indicates that the host's response to the transplantation process itself is essential for the maintenance of plasticity after monocular deprivation (Hoseini et al, 2019). It is currently unknown what exactly elicits the new plasticity in the host cortex, transient disinhibition or circuit destabilization, as well as what factors intrinsic to both host and transplanted cells may regulate this process.…”