Abstract
The end of the critical period for primary visual cortex (V1) coincides with the deposition of perineuronal nets (PNN) onto Parvalbumin (PV) inhibitory neurons. Recently, we found that transplantation of embryonic inhibitory neurons into adult V1 reinstates a new critical period. Here we used Wisteria Floribunda Agglutinin (WFA) staining to compare the deposition of PNNs onto neurons during normal development and following transplantation at equivalent cell ages. In accord with previous findings, PV and PNN expression increases from negligible levels at postnatal day 14 (P14) to mature levels by P70. In contrast to P14, PNNs are found on transplanted PV neurons by 21 days after transplantation and persist to 105 days after transplantation. This precocious deposition was specific to PV neurons and excluded transplanted neurons expressing Somatostatin. Notably, the onset of PV expression in transplanted inhibitory neurons follows the timing of PV expression in juvenile V1. Moreover, transplantation has no discernible effect on host PNNs. The precocious deposition of PNNs onto transplanted PV neurons suggests that PNN expression identified by WFA does not reflect neuronal maturity and may be an inaccurate marker for transplant-induced plasticity of cortical circuits.
Highlights
The critical period for binocular vision is a time of heightened experience-dependent plasticity in primary visual cortex[1,2]
We first quantified the expression of perineuronal nets (PNN) on inhibitory neurons before (P14), during (P28), and after (P74) the juvenile critical period for ocular dominance plasticity (P19-P32)[1] using a Wisteria Floribunda Agglutinin (WFA) stain (Fig. 1B)
The developmental timeline of PNN expression in primary visual cortex we found is comparable to previous studies[11,27]
Summary
The critical period for binocular vision is a time of heightened experience-dependent plasticity in primary visual cortex[1,2]. The disruption of PNNs and associated signaling in adult animals has been shown to restore visual cortical plasticity[9,10,14,15,16,17,18] These findings suggest that the deposition of PNNs onto PV inhibitory neurons applies the brakes to critical period plasticity. We were guided by the hypothesis that a cell intrinsic developmental program governs the reactivation of cortical plasticity by transplanted inhibitory neurons. Our results indicate that the timing of PNN deposition occurs more rapidly onto transplanted inhibitory neurons than anticipated. These findings challenge the hypothesis that PNN deposition alone is responsible for regulating the critical period
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