Figure 1. Molecular pathways involved in RA-dependent homeostatic synaptic plasticity and its interaction with Hebbian plasticity.

Left: Molecular pathways involved in RA-dependent homeostatic synaptic plasticity (HSP). A reduction in postsynaptic Ca²⁺ levels resulted from synaptic inactivity triggers RA synthesis, which disinhibits local protein synthesis and promotes synaptic insertion of AMPARs. CaN: calcineurin; RALDH: retinal dehydrogenase. Right: Exocytosis of AMPAR-containing vesicles into synaptic membranes during LTP and HSP is mediated by partially overlapping SNARE components. Postsynaptic deletion of Q-SNARE syntaxin-4 (Stx-4), which is uniquely required for HSP, prevents the impairment of LTP following RA treatment by blocking RA-induced HSP.