title: Trk B signalling controls LTP but not LTD expression in the developing rat visual cortex.
abstract: 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.
authors.affiliation: International School for Advanced Studies (SISSA), Neuroscience Programme, Via Beirut 2-4, 34014 Trieste, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Sermasi
authors.forename: E
authors.initials: E
authors.lastname: Margotti
authors.forename: A
authors.initials: A
authors.lastname: Cattaneo
authors.forename: L
authors.initials: L
authors.lastname: Domenici
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D019208:Brain-Derived Neurotrophic Factor / Q000494:pharmacology; D004594:Electrophysiology; D007074:Immunoglobulin G / Q000494:pharmacology; D017774:Long-Term Potentiation / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D009414:Nerve Growth Factors / Q000494:pharmacology; D009433:Neural Inhibition / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D020813:Receptor, trkB / Q000032:analysis / Q000276:immunology / Q000502:physiology*; D014793:Visual Cortex / Q000737:chemistry / Q000254:growth & development* / Q000502:physiology*
chemical_list: D000911:Antibodies, Monoclonal; D019208:Brain-Derived Neurotrophic Factor; D007074:Immunoglobulin G; D009414:Nerve Growth Factors; C071951:neurotrophin 5; D020813:Receptor, trkB; C073922:neurotrophin 4