Schematic view of possible roles for Sema3A in PNN related plasticity. Sema3A protein molecules (red spheres) derived from the more distant cells in the environment, that is, meningeal cell or cells of the choroid plexus, or secreted along axons or by presynaptic terminals (yellow) integrate in the PNN surrounding parvalbumin (PV) positive interneurons. PV-interneurons express Sema3A receptor components (NP1/PlxA) which may trigger an internal response upon Sema3A binding that eventually may change the properties of the PV cell (A). Alternatively, Sema3A may act on (new) presynaptic terminals. Sema3A bound to the PNN may repel growing axons (green) away from the PV cell membrane and thereby prevent the formation of new synapses between PV-interneurons and ingrowing axons (B). Sema3A in the PNN may also “stabilize” synaptic contacts on the PV-interneuron surface by preventing local rearrangements of existing synaptic terminals (C).