Synaptic Activity-Regulated Wnt Signaling in Synaptic Plasticity, Glial Function and Chronic Pain
Affiliation: Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Keywords: Wnt, pain, synapse, glia, synaptic plasticity, neuroinflammation, N-methyl-D-aspartate, receptor, mammalian target
of rapamycin, long-term potentiation, Human immunodeficiency virus-1.Wnt, pain, synapse, glia, synaptic plasticity, neuroinflammation, N-methyl-D-aspartate, receptor, mammalian target
of rapamycin, long-term potentiation, Human immunodeficiency virus-1.
Wnt signaling pathways play important roles in various developmental and oncogenic processes. In the nervous
system, Wnt signaling regulates neuronal morphogenesis and synaptic differentiation. Disturbance of Wnt signaling is
implicated in the pathogenesis of neurological diseases. Recent studies indicate that Wnt signaling in neurons is closely
coupled to synaptic activation, and that the activity-regulated Wnt signaling is critical for the expression of synaptic
plasticity and the formation of memory. Dysregulation of the activity-regulated Wnt signaling may have a significant
impact on the function of the nervous system. In this article, we will review the identified mechanisms by which synaptic
activity controls Wnt signaling in neurons and the neurological functions of the activity-regulated Wnt signaling under
normal and specific disease conditions. In particular, we will discuss the role of Wnt signaling in the pathogenesis of
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