Premium
Trk B signalling controls LTP but not LTD expression in the developing rat visual cortex
Author(s) -
Sermasi Edoardo,
Margotti Elisa,
Cattaneo Antonino,
Domenici Luciano
Publication year - 2000
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.1460-9568.2000.00014.x
Subject(s) - trk receptor , long term potentiation , tropomyosin receptor kinase b , neuroscience , neurotrophin , synaptic plasticity , endogeny , tropomyosin receptor kinase a , biology , brain derived neurotrophic factor , visual cortex , neurotrophic factors , chemistry , receptor , microbiology and biotechnology , endocrinology , biochemistry
Neurotrophins have been suggested to act as liaison molecules between activity‐dependent synaptic plasticity and the establishment of patterns of synaptic connectivity during postnatal developmental in different brain areas, including the visual cortex. In particular, recent studies have shown that Trk B ligands are involved in the formation of the ocular dominance columns during postnatal development. Here, we examined the contribution of endogenous Trk B activation to the regulation of different forms of synaptic plasticity including long‐term potentiation (LTP), long‐term depression (LTD) and LTP after LTD in the developing visual cortex. Rat cortical slices were incubated with a soluble form of Trk B receptor (TrkB IgG) preventing Trk B activation by endogenous ligands. LTP expression was also studied at P23 (postnatal), when the expression of brain‐derived neurotrophic factor (BDNF) reaches a peak and the LTP expression is normally downregulated. The present results demonstrate that Trk B activation is required for the long‐term maintenance, > 30 min, of both LTP and LTP after LTD at P17. At P23, a higher concentration of TrkB IgG was necessary to impair LTP. In contrast, neither amplitude nor duration of LTD were affected by Trk B ligands blockade. Taken together, these results indicate that endogenous Trk B ligands are necessary for the expression of LTP but not LTD at a critical time during postnatal cortical development.