Format

Send to

Choose Destination
See comment in PubMed Commons below
Trends Neurosci. 2012 May;35(5):293-304. doi: 10.1016/j.tins.2012.03.003. Epub 2012 Apr 18.

EphBs: an integral link between synaptic function and synaptopathies.

Author information

1
Department of Neuroscience and Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 462, Philadelphia, PA 19107, USA.

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.

PMID:
22516618
PMCID:
PMC3631563
DOI:
10.1016/j.tins.2012.03.003
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center