TY - JOUR T1 - TrkB Modulates Fear Learning and Amygdalar Synaptic Plasticity by Specific Docking Sites JF - The Journal of Neuroscience JO - J. Neurosci. SP - 10131 LP - 10143 DO - 10.1523/JNEUROSCI.1707-09.2009 VL - 29 IS - 32 AU - Gabriele Musumeci AU - Carla Sciarretta AU - Antonio Rodríguez-Moreno AU - Mumna Al Banchaabouchi AU - Vicente Negrete-Díaz AU - Marco Costanzi AU - Valeria Berno AU - Alexei V. Egorov AU - Oliver von Bohlen und Halbach AU - Vincenzo Cestari AU - José M. Delgado-García AU - Liliana Minichiello Y1 - 2009/08/12 UR - http://www.jneurosci.org/content/29/32/10131.abstract N2 - 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/PLCγ (phospholipase Cγ) 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. ER -