Topic: critical period

Developmental myelination is a protracted process in the mammalian brain. One theory for why oligodendrocytes mature so slowly posits that myelination may stabilize neuronal circuits and temper neuronal plasticity as animals age. We tested this theory in the visual cortex, which has a well-defined critical period for experience-dependent neuronal plasticity. During adolescence, visual experience modulated oligodendrocyte maturation in visual cortex. To determine whether oligodendrocyte maturation in turn regulates neuronal plasticity, we genetically blocked oligodendrocyte differentiation and

Postsynaptic density protein 95 (PSD-95) is an important signalling scaffold of the PSD of excitatory synapses. We have previously shown that PSD-95 dependent silent synapse maturation closes the critical period (CP) for ocular dominance plasticity in mouse V1: PSD-95 KO mice display both functional & structural hallmarks of CP plasticity and synapses cannot properly stabilize. Since the development of binocularity happens during the CP, we hypothesized that PSD-95 KOs should display compromised binocular integration. To test this hypothesis, we performed both behavioural experiments and m

Lack of lateral hypothalamic orexin/hypocretin (OH) peptides (Sathiyamani et al, accompanying poster) shortens the critical period (CP) for ocular dominance plasticity (ODP) in mouse primary visual cortex (V1). We have previously shown that altered timing of the CP for ODP is caused by modified maturation of AMPA-silent synapses in both PSD-93 and PSD-95 KO mice, and results in compromised orientation discrimination (Favaro et al 2018, PLosBiol 16:e2006838). We therefore analysed whether orexin KO modifies AMPA-currents in V1 and causes similar visual deficits.First, we quantified AMPA-recepto

Amblyopia arises from neuronal adaptation due to abnormal experience of one eye during a critical period of visual development. The molecular mechanisms underlying amblyopia are not characterized. To investigate this process, we used the monocular deprivation experimental paradigm in young rats to induce plasticity of neuronal excitability in dorsal lateral geniculate nucleus (dLGN) neurons (Duménieu et al., BioRxiv 2023). Employing a proteomic approach, we identified activity-dependent dynamic change in the components of dLGN neurons. By microdissection we isolated deprived and spared regions