PMID- 10762369 OWN - NLM STAT- MEDLINE DCOM- 20000621 LR - 20190815 IS - 0953-816X (Print) IS - 0953-816X (Linking) VI - 12 IP - 4 DP - 2000 Apr TI - Trk B signalling controls LTP but not LTD expression in the developing rat visual cortex. PG - 1411-9 AB - 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. FAU - Sermasi, E AU - Sermasi E AD - International School for Advanced Studies (SISSA), Neuroscience Programme, Via Beirut 2-4, 34014 Trieste, Italy. FAU - Margotti, E AU - Margotti E FAU - Cattaneo, A AU - Cattaneo A FAU - Domenici, L AU - Domenici L LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - France TA - Eur J Neurosci JT - The European journal of neuroscience JID - 8918110 RN - 0 (Antibodies, Monoclonal) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Immunoglobulin G) RN - 0 (Nerve Growth Factors) RN - 145172-44-7 (neurotrophin 5) RN - EC 2.7.10.1 (Receptor, trkB) RN - P658DCA9XD (neurotrophin 4) SB - IM MH - Animals MH - Antibodies, Monoclonal MH - Brain Chemistry/drug effects/physiology MH - Brain-Derived Neurotrophic Factor/pharmacology MH - Electrophysiology MH - Immunoglobulin G/pharmacology MH - Long-Term Potentiation/*physiology MH - Membrane Potentials/physiology MH - Mice MH - Mice, Inbred BALB C MH - Nerve Growth Factors/pharmacology MH - Neural Inhibition/*physiology MH - Neuronal Plasticity/physiology MH - Rats MH - Rats, Inbred Strains MH - Receptor, trkB/analysis/immunology/*physiology MH - Visual Cortex/chemistry/*growth & development/*physiology EDAT- 2000/04/13 09:00 MHDA- 2000/06/24 11:00 CRDT- 2000/04/13 09:00 PHST- 2000/04/13 09:00 [pubmed] PHST- 2000/06/24 11:00 [medline] PHST- 2000/04/13 09:00 [entrez] AID - ejn014 [pii] AID - 10.1046/j.1460-9568.2000.00014.x [doi] PST - ppublish SO - Eur J Neurosci. 2000 Apr;12(4):1411-9. doi: 10.1046/j.1460-9568.2000.00014.x.