ArticleFrontiers in molecular neuroscience2014
Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala.
Article in Frontiers in molecular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
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- Long-Term Depression Is Independent of GluN2 Subunit Composition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- NPY Induces Stress Resilience via Downregulation ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- MPTP-Induced Dopamine Depletion in Basolateral AmygdalaFrontiers in molecular neuroscience · 2017Article
- Propranolol decreases retention of fear memory by modulating the stability of surface glutamate receptor GluA1 subunits in the lateral amygdala.British journal of pharmacology · 2015Article
- NMDA Receptor-Dependent Synaptic Depression in Potentiated Synapses of the Anterior Cingulate Cortex of adult Mice.Molecular painArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced post-synaptically at the thalamic input but presynaptically at the cortical input, since post-synaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD).
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