Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 25, Pages 8367-8375Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4164-08.2010
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Funding
- Deutsche Forschungsgemeinschaft
- Fonds der Chemischen Industrie
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Ca2+ influx through postsynaptic Ca(v)1.xL-type voltage-gated channels (LTCCs) is particularly effective in activating neuronal biochemical signaling pathways that might be involved in Hebbian synaptic plasticity (i.e., long-term potentiation and depression) and learning and memory. Here, we demonstrate that Ca(v)1.2 is the functionally relevant LTCC isoform in the thalamus-amygdala pathway of mice. We further show that acute pharmacological block of LTCCs abolishes Hebbian plasticity in the thalamus-amygdala pathway and impairs the acquisition of conditioned fear. On the other hand, chronic genetic loss of Ca(v)1.2 triggers a homeostatic change of the synapse, leading to a fundamental alteration of the mechanism of Hebbian plasticity by synaptic incorporation of Ca2+-permeable, GluA2-lacking AMPA receptors. Our results demonstrate for the first time the importance of the Ca(v)1.2 LTCC subtype in synaptic plasticity and fear memory acquisition.
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