Synaptic Phospholipid Signaling Modulates Axon Outgrowth via Glutamate-dependent Ca2+-mediated Molecular Pathways.

摘要: Altered synaptic bioactive lipid signaling has been recently shown to augment neuronal excitation in the hippocampus of adult animals by activation presynaptic LPA2-receptors leading increased glutamate release. Here, we show that this results higher postsynaptic Ca2+ levels and premature onset spontaneous activity developing entorhinal cortex. Interestingly, synchronized led reduced axon growth velocity neurons which project via perforant path hippocampus. This was due Ca2+-dependent molecular affecting stabilization actin cytoskeleton. The affected entire cortical network thus overall fiber numbers mature is known be important for specific memory functions. Our data precise regulation early lipids critical importance proper circuit formation.