Research article summary (published 10 Aug 2009):

TrkB modulates fear learning and amygdalar synaptic plasticity by specific docking sites.

Full 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/PLCgamma (phospholipase Cgamma) 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.

Author information

Author/s: Musumeci, Gabriele (G); Sciarretta, Carla (C); Rodríguez-Moreno, Antonio (A); Al Banchaabouchi, Mumna (M); Negrete-Díaz, Vicente (V); Costanzi, Marco (M); Berno, Valeria (V); Egorov, Alexei V (AV); von Bohlen Und Halbach, Oliver (O); Cestari, Vincenzo (V); Delgado-García, José M (JM); Minichiello, Liliana (L);

Affiliation: Mouse Biology Unit, European Molecular Biology Laboratory, Monterotondo, Italy.

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Aug; vol 29 (issue 32) : pp 10131-43

Dates: Created 2009/08/13; Completed 2009/09/08;

PMID: 19675247, status: MEDLINE (last retrieval date: 9/8/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Amygdala - physiology Animals Binding Sites - genetics; physiology Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Conditioning, Classical - physiology Fear Hippocampus - physiology Learning - physiology Long-Term Potentiation - physiology Maze Learning - physiology Membrane Glycoproteins - genetics; metabolism

Memory - physiology Mice Mice, Mutant Strains Neuronal Plasticity - physiology Phosphorylation - physiology Point Mutation Protein-Tyrosine Kinases - genetics; metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Synapses - physiology Synaptic Transmission - physiology

Associated Chemicals: Membrane Glycoproteins (0) ; Ntrk2 protein, mouse (EC 2.7.1.112) ; Protein-Tyrosine Kinases (EC 2.7.1.112) ; Proto-Oncogene Proteins c-akt (EC 2.7.1.37) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)

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