http://www.cnr.it/ontology/cnr/individuo/prodotto/ID38712

TrkB modulates fear learning and amygdalar synaptic plasticity by specific docking sites (Articolo in rivista)

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TrkB modulates fear learning and amygdalar synaptic plasticity by specific docking sites (Articolo in rivista) (literal)

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Musumeci G, Sciarretta C, Rodríguez-Moreno A, Al Banchaabouchi M, Negrete-Díaz V, Costanzi M, Berno V, Egorov AV, von Bohlen Und Halbach O, Cestari V, Delgado-García JM, Minichiello L (2009)
TrkB modulates fear learning and amygdalar synaptic plasticity by specific docking sites
in The journal of neuroscience (Online)
(literal)

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Musumeci G, Sciarretta C, Rodríguez-Moreno A, Al Banchaabouchi M, Negrete-Díaz V, Costanzi M, Berno V, Egorov AV, von Bohlen Und Halbach O, Cestari V, Delgado-García JM, Minichiello L (literal)

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1. EMBL Mouse Biol Unit, I-00015 Monterotondo, Italy (G. Musumeci, C. Sciarretta, M. Al Banchaabouchi, V. Berno, A. , L. Minichiello) 2. Univ Pablo Olavide, Div Neurociencias, Seville 41013, Spain (V. Negrete-Díaz, J. M. Delgado-García) 3. CNR, Ist Neurosci, I-00143 Rome, Italy (Cestari, Costanzi) 4. Univ Heidelberg, Dept Neuroanat, Interdisciplinary Ctr Neurosci, D-69120 Heidelberg, Germany (V. Egorov, O. Von Bohlen und Halbach) 5. Univ Lumsa, Fac Sci Formaz, I-00193 Rome, Italy (Cestari, Costanzi) 6. Univ Edinburgh, Ctr Neuroregenerat, Edinburgh EH16 4SB, Midlothian, Scotland (Minichiello) (literal)

Titolo

TrkB modulates fear learning and amygdalar synaptic plasticity by specific docking sites (literal)

Abstract

Understanding the modulation of the neural circuitry of fear is clearly one of the most important aims in neurobiology. Protein phosphorylation in response to external stimuli is considered a major mechanism underlying dynamic changes in neural circuitry. TrkB (Ntrk2) neurotrophin receptor tyrosine kinase potently modulates synaptic plasticity and activates signal transduction pathways mainly through two phosphorylation sites [Y515/Shc site; Y816/PLC gamma (phospholipase C gamma) site]. To identify the molecular pathways required for fear learning and amygdalar synaptic plasticity downstream of TrkB, we used highly defined genetic mouse models carrying single point mutations at one of these two sites (Y515F or Y816F) to examine the physiological relevance of pathways activated through these sites for pavlovian fear conditioning (FC), as well as for synaptic plasticity as measured by field recordings obtained from neurons of different amygdala nuclei. We show that a Y816F point mutation impairs acquisition of FC, amygdalar synaptic plasticity, and CaMKII signaling at synapses. In contrast, a Y515F point mutation affects consolidation but not acquisition of FC to tone, and also alters AKT signaling. Thus, TrkB receptors modulate specific phases of fear learning and amygdalar synaptic plasticity through two main phosphorylation docking sites. (literal)

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