Visual Cortex Plasticity: A Complex Interplay of Genetic and Environmental Influences

Figure 2

The reinstatement of ocular dominance plasticity in adulthood is associated with signal transduction pathways that involve the enhanced action of either neuromodulatory projection systems (e.g., serotonin and acetylcholine) or IGF-1 signaling, which all set in motion physiological processes that modulate the inhibitory/excitatory ratio in favour of excitation [14–17, 72, 73, 83]. A shift of the inhibitory/excitatory balance may directly activate intracellular mechanisms that eventually promote epigenetic modifications of chromatin structure (e.g., changes of DNA methylation patterns and/or posttranslational modifications of histones), which in turn allow for the expression of genes that act as downstream effectors of plastic phenomena in adult life. A pharmacological reduction of intracortical inhibition enhances plasticity while promoting the activity-dependent BDNF expression (unpublished data) and degradation of extracellular matrix (ECM) components that are inhibitory for plasticity [23]. BDNF-trkB signaling might upregulate the expression of additional genes associated with functional modifications in the visual cortex. Degradation of ECM components (e.g., CSPGs) may modify the inhibition/excitation ratio in the visual system. The interaction between BDNF-trkB signaling and ECM reorganization has yet to be explored. Continuous arrows represent established interactions between the molecular and cellular processes mentioned (boxes). Dashed lines represent interactions that remain to be ascertained.