Journal
TRENDS IN NEUROSCIENCES
Volume 35, Issue 5, Pages 293-304Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2012.03.003
Keywords
Alzheimer's disease; neuropathic pain; synaptogenesis; NMDA receptors; receptor tyrosine kinase; ephrin
Categories
Funding
- National Eye Institute [EY007035]
- Dana Foundation, National Institute on Drug Abuse [DA022727]
- National Institute of Mental Health [MH086425]
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The assembly and function of neuronal circuits rely on selective cell cell interactions to control axon targeting, generate pre- and postsynaptic specialization and recruit neurotransmitter receptors. In neurons, EphB receptor tyrosine kinases mediate excitatory synaptogenesis early during development, and then later coordinate synaptic function by controlling synaptic glutamate receptor localization and function. EphBs direct synapse formation and function to regulate cellular morphology through downstream signaling mechanisms and by interacting with glutamate receptors. In humans, defective EphB-dependent regulation of NMDA receptor (NMDAR) localization and function is associated with neurological disorders, including neuropathic pain, anxiety disorders and Alzheimer's disease (AD). Here, we propose that EphBs act as a central organizer of excitatory synapse formation and function, and as a key regulator of diseases linked to NMDAR dysfunction.
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