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Effect of heparin‐binding growth‐associated molecule (HB‐GAM) on synaptic transmission and early LTP in rat hippocampal slices
Author(s) -
Sari E. Lauri,
Heikki Rauvala,
Kai Kaila,
Tomi Taira
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00039.x
Subject(s) - long term potentiation , synaptogenesis , hippocampal formation , nmda receptor , synaptic plasticity , chemistry , neurotransmission , neuroscience , neurite , hippocampus , synapse , ampa receptor , microbiology and biotechnology , biology , receptor , biochemistry , in vitro
Heparin‐binding growth‐associated molecule (HB‐GAM) is an 18‐kDa developmentally regulated protein, which promotes neurite outgrowth, axonal guidance and synaptogenesis through interaction with cell‐surface heparan‐sulphate proteoglycans. We have studied the effect of HB‐GAM on synaptic transmission and long‐term potentiation (LTP) in the area CA1 of rat hippocampal slices, where HB‐GAM mRNA is expressed in an activity‐dependent manner. Injection of recombinant HB‐GAM into the dendritic area inhibited tetanus‐induced LTP without affecting baseline synaptic responses or the N ‐methyl‐ d ‐aspartate (NMDA)‐receptor mediated transmission. HB‐GAM did not depotentiate tetanus‐induced LTP or prevent heterosynaptic LTP induced by application of tetraethylammonium (TEA), indicating that the effect was limited to early, synapse‐specific stages of LTP induction. These results suggest that HB‐GAM is involved in the regulation of synaptic plasticity in hippocampus.