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The Journal of Neuroscience, February 15, 1999, 19(4):1226-1235
Reg1ulatory Role and Molecular Interactions of a Cell-Surface
Heparan Sulfate Proteoglycan (N-syndecan) in
Hippocampal Long-Term Potentiation
S. E.
Lauri1, 2,
S.
Kaukinen2,
T.
Kinnunen2,
A.
Ylinen3,
S.
Imai2,
K.
Kaila1,
T.
Taira1, and
H.
Rauvala2
1 Department of Biosciences, Division of Animal
Physiology, 00014 University of Helsinki, Helsinki, Finland,
2 Laboratory of Molecular Neurobiology, Institute of
Biotechnology and Department of Biosciences, 00014 University of
Helsinki, Helsinki, Finland, and 3 A. I. Virtanen
Institute and Department of Neuroscience and Neurology, University of
Kuopio, 70211 Kuopio, Finland
The cellular mechanisms responsible for synaptic plasticity involve
interactions between neurons and the extracellular matrix. Heparan
sulfates (HSs) constitute a group of glycosaminoglycans that accumulate
in the  -amyloid deposits in Alzheimer's disease and influence the
development of neuron-target contacts by interacting with other cell
surface and matrix molecules. However, the contribution of HSs to brain
function is unknown. We found that HSs play a crucial role in long-term
potentiation (LTP), a finding that is consistent with the idea that
converging molecular mechanisms are used in the development of
neuron-target contacts and in activity-induced synaptic plasticity in
adults. Enzymatic cleavage of HS by heparitinase as well as addition of
soluble heparin-type carbohydrates prevented expression of LTP in
response to 100 Hz/1 sec stimulation of Schaffer collaterals in rat
hippocampal slices. A prominent carrier protein for the type of glycans
implicated in LTP regulation in the adult hippocampus was identified as
N-syndecan (syndecan-3), a transmembrane proteoglycan
that was expressed at the processes of the CA1 pyramidal neurons in an
activity-dependent manner. Addition of soluble
N-syndecan into the CA1 dendritic area prevented
tetanus-induced LTP. A major substrate of src-type kinases, cortactin
(p80/85), and the tyrosine kinase fyn copurified with
N-syndecan from hippocampus. Moreover, association of
both cortactin and fyn to N-syndecan was rapidly increased after induction of LTP. N-syndecan may thus
act as an important regulator in the activity-dependent modulation of
neuronal connectivity by transmitting signals between extracellular
heparin-binding factors and the fyn signaling pathway.
Key words:
long-term potentiation; synaptic plasticity; extracellular matrix; heparan sulfate proteoglycans; hippocampus; src
family tyrosine kinases; cortactin
Copyright © 1999 Society for Neuroscience 0270-6474/99/1941226-10$05.00/0
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