PubMed 20573883
Referenced in: none
Automatically associated channels: Cav1.2
Title: Homeostatic switch in hebbian plasticity and fear learning after sustained loss of Cav1.2 calcium channels.
Authors: Nicole Langwieser, Carl J Christel, Thomas Kleppisch, Franz Hofmann, Carsten T Wotjak, Sven Moosmang
Journal, date & volume: J. Neurosci., 2010 Jun 23 , 30, 8367-75
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20573883
Abstract
Ca(2+) influx through postsynaptic Ca(v)1.x L-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 Ca(2+)-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.