AI Article Synopsis
- Neuronal circuits rely on selective interactions for axon targeting, synaptic specialization, and neurotransmitter receptor recruitment, with EphB receptor tyrosine kinases playing a key role in this process.
- EphB receptors are involved in excitatory synapse formation early in development and later help regulate synaptic function by influencing glutamate receptor localization.
- Defects in EphB function are linked to various neurological disorders, including neuropathic pain, anxiety, and Alzheimer's disease, highlighting their importance in synaptic organization and NMDAR-related diseases.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631563 | PMC |
| http://dx.doi.org/10.1016/j.tins.2012.03.003 | DOI Listing |
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