Dark exposure affects plasticity‐related molecules and interneurons throughout the visual system during adulthood

Abstract

Several experimental manipulations, including visual deprivation, are able to induce critical period‐like plasticity in the visual cortex of adult animals. In this regard, many studies have analyzed the effects of dark exposure in adult animals, but still little is known about the role of interneurons and plasticity‐related molecules on such mechanisms. In this study, we analyzed the effects of 10 days of dark exposure on the connectivity and structure of interneurons, both in the primary visual cortex and in the rest of cerebral regions implicated in the transmission of visual stimulus. We found that this environmental manipulation induces changes in the expression of synaptic molecules throughout the visual pathway and in the structure of interneurons in the primary visual cortex. Moreover, we found altered expression in the polysialylated form of the neural cell adhesion molecule and in perineuronal nets surrounding parvalbumin expressing interneurons, suggesting that these plasticity‐related molecules may be involved in the changes produced by dark exposure. Together, our findings indicate that dark exposure produces an important alteration of inhibitory circuits and molecules related to their plasticity, not only in the visual cortex but throughout the visual pathway.

Fine structure analysis of perineuronal nets in the ketamine model of schizophrenia

“…The accumulation of PNNs around PV+ cells acts as a molecular brake on synaptic plasticity and marks the closing of critical periods of plasticity (Sigal et al., 2019). Moreover, the increase in the expression of parvalbumin has been directly linked to increased activity of parvalbumin cells that might result into activity‐dependent accumulation of PNN and hence marks the maturation of inhibitory cortical circuitry (Carceller, Guirado, & Nacher, 2019; Dityatev et al., 2007; Favuzzi et al., 2017; Patz, Grabert, Gorba, Wirth, & Wahle, 2004). Interestingly, we also observed a moderate but significant positive correlation of the number of PNN units, circularity and solidity of ECM in 2D with either intensity or the size of PV + cells after the treatment with ketamine, suggesting the treatment induces modification in PNNs depending on the level of PV+ cell activity and subtype.…”

Management of Abnormal Visual Developments

“…It has been concluded that the reduction of inhibition in the visual cortex is the core to restore the plasticity of adult amblyopia after the critical period. Studies on animal models have shown that reducing GABAergic inhibition with pharmacological treatment such as blockers of GABA synthesis or GABA receptor antagonists or environmental paradigms which contain environment enrichment and dark exposure can increase plasticity in the adult brain, enabling ocular dominance plasticity and favoring recovery from amblyopia [112][113][114]. New research has found that transplanted embryonic inhibitory neurons from the medial ganglionic eminence reinstate ocular dominance plasticity in adult amblyopic mice, with the recovery of both visual cortical responses and performance on a behavioral test of visual acuity [115].…”