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Published 22 December 2003. doi:10.1083/jcb.200306033
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© The Rockefeller University Press, 0021-9525/2003/12/1313 $8.00
The Journal of Cell Biology, Volume 163, Number 6, 1313-1326

Article

Multiple EphB receptor tyrosine kinases shape dendritic spines in the hippocampus



Mark Henkemeyer3, Olga S. Itkis1, Michelle Ngo1, Peter W. Hickmott2 and Iryna M. Ethell1

1 Division of Biomedical Sciences, University of California Riverside, Riverside, CA 92521
2 Department of Psychology, University of California Riverside, Riverside, CA 92521
3 Center for Developmental Biology and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390

Address correspondence to Iryna M. Ethell, Division of Biomedical Sciences, University of California Riverside, Riverside, CA 92521. Tel.: (909) 787-2186. Fax: (909) 827-7121. email: iryna.ethell{at}ucr.edu

Here, using a genetic approach, we dissect the roles of EphB receptor tyrosine kinases in dendritic spine development. Analysis of EphB1, EphB2, and EphB3 double and triple mutant mice lacking these receptors in different combinations indicates that all three, although to varying degrees, are involved in dendritic spine morphogenesis and synapse formation in the hippocampus. Hippocampal neurons lacking EphB expression fail to form dendritic spines in vitro and they develop abnormal spines in vivo. Defective spine formation in the mutants is associated with a drastic reduction in excitatory glutamatergic synapses and the clustering of NMDA and AMPA receptors. We show further that a kinase-defective, truncating mutation in EphB2 also results in abnormal spine development and that ephrin-B2–mediated activation of the EphB receptors accelerates dendritic spine development. These results indicate EphB receptor cell autonomous forward signaling is responsible for dendritic spine formation and synaptic maturation in hippocampal neurons.

Key Words: dendritic spine morphogenesis; hippocampal neuron; postsynaptic; receptor signaling; synapse

The online version of this article contains supplemental material.

Abbreviations used in this paper: AMPAR, AMPA receptor; DIV, days in vitro; GABA, {gamma}-aminobutyric acid; GAD, glutamic acid decarboxylase; GluR, glutamate receptor; IR, immunoreactivity; KO, knockout; LIMK, LIM kinase; NMDAR, NMDA receptor; PSD, post-synaptic density; WT, wild type.


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