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The Journal of Neuroscience, March 31, 2004, 24(13):3281-3288; doi:10.1523/JNEUROSCI.5303-03.2004

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Behavioral/Systems/Cognitive
Pavlovian Fear Conditioning Regulates Thr²⁸⁶ Autophosphorylation of Ca²+/Calmodulin-Dependent Protein Kinase II at Lateral Amygdala Synapses

Sarina M. Rodrigues,¹ Claudia R. Farb,¹ Elizabeth P. Bauer,¹ Joseph E. LeDoux,¹ and Glenn E. Schafe²

¹W. M. Keck Foundation Laboratory of Neurobiology, Center for Neural Science, New York University, New York, New York 10003, and ²Department of Psychology, Yale University, New Haven, Connecticut 06520

Ca²+/calmodulin-dependent protein kinase II (CaMKII) plays a critical role in synaptic plasticity and memory formation in a variety of learning systems and species. The present experiments examined the role of CaMKII in the circuitry underlying pavlovian fear conditioning. First, we reveal by immunocytochemical and tract-tracing methods that CaMKII is postsynaptic to auditory thalamic inputs and colocalized with the NR2B subunit of the NMDA receptor. Furthermore, we show that fear conditioning results in an increase of the autophosphorylated (active) form of CaMKII in lateral amygdala (LA) spines. Next, we demonstrate that intra-amygdala infusion of a CaMK inhibitor, 1-[NO-bis-1,5-isoquinolinesulfonyl]-N-methyl-L-tyrosyl-4-phenylpiperazine, KN-62, dose-dependently impairs the acquisition, but not the expression, of auditory and contextual fear conditioning. Finally, in electrophysiological experiments, we demonstrate that an NMDA receptor-dependent form of long-term potentiation at thalamic input synapses to the LA is impaired by bath application of KN-62 in vitro. Together, the results of these experiments provide the first comprehensive view of the role of CaMKII in the amygdala during fear conditioning.

Key words: CaMKII; fear; phosphorylation; LTP; plasticity; translocation

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Received June 30, 2003; revised January 20, 2004; accepted January 23, 2004.

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