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The EphA4 receptor regulates dendritic spine remodeling by affecting β1-integrin signaling pathways

Bourgin, Caroline, Murai, Keith K., Richter, Melanie, Pasquale, Elena B.·2007·The Journal of Cell Biology
DOI 10.1083/jcb.200610139PMC PMC2064660
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Abstract

Remodeling of dendritic spines is believed to modulate the function of excitatory synapses. We previously reported that the EphA4 receptor tyrosine kinase regulates spine morphology in hippocampal pyramidal neurons, but the signaling pathways involved were not characterized (Murai, K.K., L.N. Nguyen, F. Irie, Y. Yamaguchi, and E.B. Pasquale. 2003. Nat. Neurosci. 6:153–160). In this study, we show that EphA4 activation by ephrin-A3 in hippocampal slices inhibits integrin downstream signaling pathways. EphA4 activation decreases tyrosine phosphorylation of the scaffolding protein Crk-associated substrate (Cas) and the tyrosine kinases focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) and also reduces the association of Cas with the Src family kinase Fyn and the adaptor Crk. Consistent with this, EphA4 inhibits β1-integrin activity in neuronal cells. Supporting a functional role for β1 integrin and Cas inactivation downstream of EphA4, the inhibition of integrin or Cas function induces spine morphological changes similar to those associated with EphA4 activation. Furthermore, preventing β1-integrin inactivation blocks the effects of EphA4 on spines. Our results support a model in which EphA4 interferes with integrin signaling pathways that stabilize dendritic spines, thus modulating synaptic interactions with the extracellular environment.

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  • β1-integrin localizes to postsynaptic sites in hippocampal neurons and influences cytoskeletal organization, dendritic spine maturation, and synaptic transmission.

    “It localizes to postsynaptic sites in hippocampal neurons and influences cytoskeletal organization, dendritic spine maturation, and synaptic transmission”

    From PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity (2025) · cites this paper as Bourgin et al., 2007

    The Discussion (page unavailable) places β1-integrin in dendritic spines of cultured hippocampal neurons and links β1-containing integrins to spine remodeling. It also associates integrin inactivation with defects in actin polymerization and synaptic plasticity, but treats an effect of the resulting spine-shape changes on synaptic transmission as a question for future study. Thus the claim's unqualified assertion about synaptic transmission goes beyond what this paper establishes. (LLM, conf=0.84)

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Metadata

Authors
Bourgin, C., Murai, K. K., Richter, M., & Pasquale, E. B.
Affiliations
  • 1Burnham Institute for Medical Research, La Jolla, CA 92037
  • 2Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, McGill University Health Centre, Montreal General Hospital, Quebec H3G 1A4, Canada
Venue
The Journal of Cell Biology
Publisher
Rockefeller University Press
Published
2007-09-17
Volume
178
Issue
7
Pages
1295-1307
ISSN
  • 1540-8140
  • 0021-9525
DOI
10.1083/jcb.200610139
PMC
PMC2064660
Cited by
136
References
12
Language
en

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