Emerging roles for semaphorins and VEGFs in synaptogenesis and synaptic plasticity

Abstract

Synapse formation, maintenance and plasticity are critical for the correct function of the nervous system and its target organs. During development, these processes enable the establishment of appropriate neural circuits. During adulthood, they allow adaptation to both physiological and environmental changes. In this review, we discuss emerging roles for two families of classical axon and vascular guidance cues in synaptogenesis and synaptic plasticity, the semaphorins and the vascular endothelial growth factors (VEGFs). Their contribution to synapse formation and function add a new facet to the spectrum of overlapping and complementary roles for these molecules in development, adulthood and disease.

Sustained Delivery of VEGF Maintains Innervation and Promotes Reperfusion in Ischemic Skeletal Muscles Via NGF/GDNF Signaling

“…5 While distal maintenance of ischemic axons does not imply enhanced functionality since those axons cannot reconnect to the cell body to resume signaling, VEGF delivery may also modulate synapses dependent on VEGF signaling. 31 This ability of VEGF to maintain synapses that would otherwise be lost due to changes at the motor end plates, which also may occur in neurodegeneration and as a result of aging, 6 may have therapeutic implications.…”

Rapid Modulation of Protein Expression in the Rat Hippocampus Following Deep Brain Stimulation of the Fornix

“…VEGF is a well-known cellular mitogen and a vascular growth factor. In addition to its pro-angiogenic activity, studies have revealed neurotrophic and neuroprotective potentials of this growth factor [56]. VEGF is implicated in the differentiation and formation of blood vessels in the brain as well as in neurogenesis [57,58].…”

Proteomic analyses of brain tumor cell lines amidst the unfolded protein response

“…There were 105 and 143 significantly scoring pathways in the U87MG and UPN933 datasets, respectively. Notable pathways in common include predicted stressed reductions in eIF2 signaling (as might be expected with UPR-induced eIF2α phosphorylation), and reductions in semaphorin signaling indicative of de-differentiation [29]. Pathways in common that displayed increased scores in the stressed state include those with few cited connections to the UPR such as CDK5 signaling, tight junction signaling, and telomerase signaling.…”