Molecular Mechanisms at the Basis of Plasticity in the Developing Visual Cortex: Epigenetic Processes and Gene Programs

Abstract

Neuronal circuitries in the mammalian visual system change as a function of experience. Sensory experience modifies neuronal networks connectivity via the activation of different physiological processes such as excitatory/inhibitory synaptic transmission, neurotrophins, and signaling of extracellular matrix molecules. Long-lasting phenomena of plasticity occur when intracellular signal transduction pathways promote epigenetic alterations of chromatin structure that regulate the induction of transcription factors that in turn drive the expression of downstream targets, the products of which then work via the activation of structural and functional mechanisms that modify synaptic connectivity. Here, we review recent findings in the field of visual cortical plasticity while focusing on how physiological mechanisms associated with experience promote structural changes that determine functional modifications of neural circuitries in V1. We revise the role of microRNAs as molecular transducers of environmental stimuli and the role of immediate early genes that control gene expression programs underlying plasticity in the developing visual cortex.

“GAG-ing with the neuron”: The role of glycosaminoglycan patterning in the central nervous system

“…This closure correlates with the formation of PNNs. PNNs are reticular structures that result from the aggregation of ECM macromolecules around the proximal neurite and cell body, particularly around inhibitory GABAergic parvalbumin-expressing interneurons whose maturation is one of the factors controlling plasticity (Hensch, 2005;Maya-Vetencourt and Pizzorusso, 2013). A reduction in PNNs number is also associated with schizophrenia (Berretta et al, 2015).…”

Role of MicroRNA in Governing Synaptic Plasticity

“…Interestingly, miRNA-132/212 also act on the synaptic plasticity of visual cortex [ 60 – 62 ]. It has been found that monocular deprivation would be in a position to hinder the modification of miRNA-132/212 locus and subsequently decreased the miRNA-132/212 cluster transcription in developing visual cortex [ 60 ].…”

“…Likewise, parallel findings revealed that the expression of miRNA-132 in the visual cortex was upregulated by light stimulation and delayed in response to dark-rearing. Inhibition of miRNA-132 can prevent dendritic spine maturation, ocular dominance plasticity, and formation of synaptic connectivity in vivo [ 61 , 62 ].…”

Prognosis and Treatment of Visual Field Defects

“…34 Experience-dependent modifications of the neuronal circuitries implying neuroplasticity were demonstrated in the mammalian and rodent visual systems. Proposed mechanisms include epigenetic alteration of chromatin structure, leading to modification of synaptic connectivity and neural circuitry in the mammalian striate cortex 35,36 and remodeling of neuronal pathways. 36,37 Impact of Visual Field Defects…”