structural:scholar_edition
Critical period opening

Critical periods of plasticity occur in the prenatal brain and continue throughout childhood until adolescence and are very limited during adulthood. Two major factors influence the opening of critical periods: cellular events (i.e. changes in molecular landscape) and sensory experience (i.e. hearing sound, visual input, etc.). Both need to coincide for the critical period to open properly. At the cellular level, critical periods are characterized by maturation of the inhibitory circuits. More precisely, factors such as brain-derived neurotrophic factor (BDNF) and orthodenticle homeobox 2 (Otx2) contribute to the maturation of a major class of inhibitory neurons: parvalbumin -positive interneurons (PV cells). Prior to the onset of the critical period, modulation of this circuit is hampered by early factors such as polysialic acid (PSA). PSA acts, in part, by preventing Otx2 interaction with PV cells. Soon after the opening of the critical period, PSA levels decrease, allowing PV cell maturation by activating inhibitory GABAa receptors that facilitate inhibitory circuit remodeling. Artificially removing PSA, or experimentally manipulating inhibitory transmission can result in early opening of the critical period. While the timing of these molecular events seems to be partially explained by clock genes, experience is crucial as sensory deprivation experiments have been shown to interfere with the proper timing of critical periods.