Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 13, Pages 3281-3288Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5303-03.2004
Keywords
CaMKII; fear; phosphorylation; LTP; plasticity; translocation
Categories
Funding
- NIMH NIH HHS [MH 11902, R01 MH046516, F32 MH011902, MH 39774, MH 00956, MH 570161, MH 46516] Funding Source: Medline
Ask authors/readers for more resources
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 alphaCaMKII 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 alphaCaMKII 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available