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The Journal of Neuroscience, February 27, 2008, 28(9):2089-2098; doi:10.1523/JNEUROSCI.5156-07.2008

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Development/Plasticity/Repair
Enhanced Cortico-Amygdala Efficacy and Suppressed Fear in Absence of Rap1

Bing-Xing Pan,^1,3 Francois Vautier,¹ Wataru Ito,¹ Vadim Y. Bolshakov,² and Alexei Morozov¹

¹Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, ²McLean Hospital, Department of Psychiatry, Harvard Medical School, Belmont, Massachusetts 02478, and ³Department of Anatomy and Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China

Correspondence should be addressed to Dr. Alexei Morozov, Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892. Email: morozova{at}mail.nih.gov

Auditory fear conditioning, a model for fear learning, is thought to be mediated by synaptic changes in the cortical and thalamic inputs to the lateral amygdala (LA); however, the specific roles of both pathways are still debated. Here, we report that a CaMKII--Cre-mediated knock-out (KO) of the rap1a and rap1b genes impaired synaptic plasticity and increased basal synaptic transmission in the cortical but not thalamic input to the LA via presynaptic changes: increases in glutamate release probability and the number of glutamate quanta released by a single action potential. Moreover, KO mice with alterations in the cortico-LA pathway had impaired fear learning, which could be rescued by training with a more aversive unconditional stimulus. These results suggest that Rap1-mediated suppression of synaptic transmission enables plasticity in the cortico-amygdala pathway, which is required for fear learning with a moderately aversive unconditional stimulus.

Key words: amygdala; fear; LTP; Rap1; cortex; thalamus

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Received Aug. 20, 2007; revised Dec. 26, 2007; accepted Jan. 12, 2008.

Correspondence should be addressed to Dr. Alexei Morozov, Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892. Email: morozova{at}mail.nih.gov

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