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• W1570680076 abstract "The classic example of experience-dependent corticalplasticity is the ocular dominance (OD) shift in visual cortexfollowing monocular deprivation (MD). As in other mammals withbinocular vision, MD in mice induces bidirectional plasticity:rapid weakening of responses evoked through the deprived eye isfollowed by delayed strengthening of open-eye responses. It hasbeen proposed that these bidirectional changes occur through threedistinct processes. First, deprived-eye responses rapidly weakenthrough homosynaptic long-term depression (LTD). As the period ofdeprivation progresses, the modification threshold determining theboundary between synaptic depression and synaptic potentiationbecomes lower via a decrease in the ratio of NR2A to NR2BN-methyl-d-aspartate receptor (NMDAR) subunits. Facilitated by thedecreased modification threshold, open-eye responses arestrengthened via homosynaptic longterm potentiation (LTP). Oneestablished LTD mechanism is a loss of sensitivity to theneurotransmitter glutamate caused by internalization ofpostsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acidreceptors (AMPARs). Although it has been shown that MD similarlycauses a loss of AMPARs from visual cortical synapses, thecontribution of this change to OD plasticity has not beenestablished. Here we develop a herpes-simplex virus (HSV) vector toexpress a peptide (G2CT) in visual cortical neurons designed toblock AMPAR internalization by hindering the association of theC-terminal tail of the AMPAR GluR2 subunit with the AP2 clathrinadaptor complex. We find that G2CT expression interferes withNMDAR-dependent AMPAR endocytosis and LTD, without affectingbaseline synaptic transmission. When expressed in vivo, G2CTcompletely blocks the MD-induced depression of deprived-eyeresponses after MD without affecting baseline visual responsivenessor experience-dependent response potentiation in layer 4 of visualcortex. Additionally, we find that OD plasticity in layer 2/3 canoccur in the absence of plasticity in layer 4, demonstrating theindependence of OD plasticity across laminae. These data suggestthat AMPAR internalization is essential for the loss of synapticstrength in layer 4 of the visual cortex following MD. This findingillustrates a critical role for LTD mechanisms in the physiologicalresponse to sensory deprivation, thereby suggesting potentialtherapeutic strategies in the treatment ofamblyopia." @default.
• W1570680076 created "2016-06-24" @default.
• W1570680076 creator A5015263495 @default.
• W1570680076 date "2010-01-01" @default.
• W1570680076 modified "2023-09-28" @default.
• W1570680076 title "Requirement for AMPA receptor endocytosis and long-term depression in ocular dominance plasticity" @default.
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