Topic: ocular dominance plasticity

Monocular deprivation-induced ocular dominance plasticity (MD-ODP) in the visual cortex is an established in vivo paradigm, in which inactivity-induced synaptic plasticity contributes to the functional reconfiguration of cortical networks. Bassoon (Bsn) is a presynaptic protein involved in the spatial and functional organisation of synaptic vesicle (SV) recycling. Here, we report a novel role for Bsn in the inactivity-induced functional reconfiguration of adult neocortical networks in vivo and in vitro. We subjected Bsn knock-out mice to MD and imaged visual stimulus-evoked intrinsic signals i

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

Lateral hypothalamic orexin/hypocretin (OH) circuits enhance exploratory behaviour and cortical gamma power, key physiological variables affecting neuronal responses in the primary visual cortex (V1). In order to elucidate the functional significance of OH signals for V1 experience-dependent plasticity, we tested orexin KO-mice in the classic ocular dominance plasticity (ODP) paradigm using intrinsic signal optical imaging (OI). Since ODP depends on age and housing conditions, we tested ODP during the critical period (CP) for ODP (P21-P35) and in adults (>P110) with standard cage (SC) housi

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