Sahún, IgnasiDelgado García, José M.Amador Arjona, AlejandroGiralt Torroella, AlbertAlberch i Vié, Jordi, 1959-Dierssen, MaraGruart i Massó, Agnès2024-02-162024-02-162007-02-280270-6474https://hdl.handle.net/2445/207666Neurotrophins and their cognate receptors might serve as feedback regulators for the efficacy of synaptic transmission.Weanalyzed mice</p><p>overexpressing TrkC (TgNTRK3) for synaptic plasticity and the expression of glutamate receptor subunits. Animals were conditioned</p><p>using a trace [conditioned stimulus (CS), tone; unconditioned stimulus (US), shock] paradigm. A single electrical pulse presented to the</p><p>Schaffer collateral– commissural pathway during the CS–US interval evoked a monosynaptic field EPSP (fEPSP) at ipsilateral CA1</p><p>pyramidal cells. In wild types, fEPSP slopes increased across conditioning sessions and decreased during extinction, being linearly</p><p>related to learning evolution. In contrast, fEPSPs in TgNTRK3 animals reached extremely high values, not accompanied with a proportionate</p><p>increase in their learning curves. Long-term potentiation evoked in conscious TgNTRK3 was also significantly longer lasting than</p><p>in wild-type mice. These functional alterations were accompanied by significant changes inNR1andNR2BNMDAreceptor subunits, with</p><p>no modification of NR1Ser 896 or NR1Ser 897 phosphorylation. No changes of AMPA and kainate subunits were detected. Results indicate</p><p>that the NT-3/TrkC cascade could regulate synaptic transmission and plasticity through modulation of glutamatergic transmission at the</p><p>CA3–CA1 synapse.8 p.application/pdfengcc-by-nc-sa (c) Sahún, I. et al., 2007http://creativecommons.org/licenses/by-nc-sa/4.0/NeuronesNeuroplasticitatRatolins transgènicsNeuronsNeuroplasticityTransgenic miceinfo:eu-repo/semantics/article5477252024-02-16info:eu-repo/semantics/openAccess