Format

Send to

Choose Destination
Exp Cell Res. 2015 Jul 15;335(2):269-78. doi: 10.1016/j.yexcr.2015.05.007. Epub 2015 May 16.

Plexin-B3 suppresses excitatory and promotes inhibitory synapse formation in rat hippocampal neurons.

Author information

1
Department of Gene Technology, Tallinn University of Technology, Tallinn, Estonia; Competence Centre for Cancer Research, Tallinn, Estonia.
2
Competence Centre for Cancer Research, Tallinn, Estonia.
3
Department of Gene Technology, Tallinn University of Technology, Tallinn, Estonia.
4
Department of Gene Technology, Tallinn University of Technology, Tallinn, Estonia; Competence Centre for Cancer Research, Tallinn, Estonia. Electronic address: andres.veske@ttu.ee.

Abstract

Molecular mechanisms underlying synaptogenesis and synaptic plasticity have become one of the main topics in neurobiology. Increasing evidence suggests that axon guidance molecules including semaphorins and plexins participate in synapse formation and elimination. Although class B plexins are widely expressed in the brain, their role in the nervous system remains poorly characterized. We previously identified that B-plexins modulate microtubule dynamics and through this impact dendrite growth in rat hippocampal neurons. Here, we demonstrate that Plexin-B2 and Plexin-B3 are present in dendrites, but do not localize in synapses. We find that overexpression of all B-plexins leads to decreased volume of excitatory synapses, and at the same time Plexin-B1 and Plexin-B3 promote inhibitory synapse assembly. Plexin-B3 mutants revealed that these processes use different downstream pathways. While elimination of excitatory synapses is the result of Plexin-B3 binding to microtubule end binding proteins EB1 and EB3, the increase in inhibitory synapses is mediated by regulation of Ras and Rho GTPases. Overall, our findings demonstrate that Plexin-B3 contributes to regulating synapse formation.

KEYWORDS:

EB3; Neurodevelopment; Neuron; Plexin; Synapse; semaphorin

PMID:
25989221
DOI:
10.1016/j.yexcr.2015.05.007
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center