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The Journal of Neuroscience, February 28, 2007, 27(9):2253-2260; doi:10.1523/JNEUROSCI.4055-06.2007

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Behavioral/Systems/Cognitive
Dissociation between CA3–CA1 Synaptic Plasticity and Associative Learning in TgNTRK3 Transgenic Mice

Ignasi Sahún,¹ José María Delgado-García,² Alejandro Amador-Arjona,¹ Albert Giralt,³ Jordi Alberch,³ Mara Dierssen,¹ and Agnès Gruart²

¹Genes and Disease Program, Genomic Regulation Center, Universidad Pompeu Fabra, Barcelona Biomedical Research Park, 08003 Barcelona, Spain, ²División de Neurociencias, Universidad Pablo de Olavide, 41013 Sevilla, Spain, and ³Department of Cell Biology and Pathology, Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, 08036 Barcelona, Spain

Correspondence should be addressed to Prof. José M. Delgado-García, División de Neurociencias, Universidad Pablo de Olavide, Carretera de Utrera, Km. 1, 41013 Sevilla, Spain. Email: jmdelgar{at}upo.es

Neurotrophins and their cognate receptors might serve as feedback regulators for the efficacy of synaptic transmission. We analyzed mice overexpressing TrkC (TgNTRK3) for synaptic plasticity and the expression of glutamate receptor subunits. Animals were conditioned using a trace [conditioned stimulus (CS), tone; unconditioned stimulus (US), shock] paradigm. A single electrical pulse presented to the Schaffer collateral–commissural pathway during the CS–US interval evoked a monosynaptic field EPSP (fEPSP) at ipsilateral CA1 pyramidal cells. In wild types, fEPSP slopes increased across conditioning sessions and decreased during extinction, being linearly related to learning evolution. In contrast, fEPSPs in TgNTRK3 animals reached extremely high values, not accompanied with a proportionate increase in their learning curves. Long-term potentiation evoked in conscious TgNTRK3 was also significantly longer lasting than in wild-type mice. These functional alterations were accompanied by significant changes in NR1 and NR2B NMDA receptor subunits, with no modification of NR1^{Ser 896} or NR1^{Ser 897} phosphorylation. No changes of AMPA and kainate subunits were detected. Results indicate that the NT-3/TrkC cascade could regulate synaptic transmission and plasticity through modulation of glutamatergic transmission at the CA3–CA1 synapse.

Key words: long-term potentiation; neurotrophins; NMDA; NT-3; TrkC; eyeblink conditioning

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Received Sept. 17, 2006; revised Jan. 20, 2007; accepted Jan. 24, 2007.

Correspondence should be addressed to Prof. José M. Delgado-García, División de Neurociencias, Universidad Pablo de Olavide, Carretera de Utrera, Km. 1, 41013 Sevilla, Spain. Email: jmdelgar{at}upo.es

This article has been cited by other articles:

				C. Gil-Sanz, J. M. Delgado-Garcia, A. Fairen, and A. Gruart Involvement of the mGluR1 Receptor in Hippocampal Synaptic Plasticity and Associative Learning in Behaving Mice Cereb Cortex, July 1, 2008; 18(7): 1653 - 1663. [Abstract] [Full Text] [PDF]

				J. M. Mercader, E. Saus, Z. Aguera, M. Bayes, C. Boni, A. Carreras, E. Cellini, R. de Cid, M. Dierssen, G. Escaramis, et al. Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders Hum. Mol. Genet., May 1, 2008; 17(9): 1234 - 1244. [Abstract] [Full Text] [PDF]

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