ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2015
The Membrane Proximal Region of AMPA Receptors in Lateral Amygdala is Essential for Fear Memory Formation.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Restoration of nNOS Expression Rescues Autistic-Like Phenotypes Through Normalization of AMPA Receptor-Mediated Neurotransmission.Molecular neurobiology · 2024Article
- Vasoactive intestinal peptide axis is dysfunctional in patients with Graves' disease.Scientific reports · 2020Article
- Learning Promotes Subfield-Specific Synaptic Diversity in Hippocampal CA1 Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Opioid receptors inhibit the spinal AMPA receptor CaExperimental neurology · 2019Article
- Genome-wide association study identifies glutamate ionotropic receptor GRIA4 as a risk gene for comorbid nicotine dependence and major depression.Translational psychiatry · 2018Article
- β-Adrenergic Receptors Regulate the Acquisition and Consolidation Phases of Aversive Memory Formation Through Distinct, Temporally Regulated Signaling Pathways.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Brain region-specific effects of cGMP-dependent kinase II knockout on AMPA receptor trafficking and animal behavior.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
- The Role of Actin Cytoskeleton in Memory Formation in Amygdala.Frontiers in molecular neuroscience · 2016Review
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Authors and funding
4 authors.
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Abstract
The membrane proximal region (MPR) of AMPA receptor (AMPAR) is needed for receptor trafficking and synaptic plasticity. However, its roles in long-term memory formation are not known. To assess the possible roles of AMPAR-MPR in rat lateral amygdala (LA) in short- and long-term fear memory formation, we used glutamate receptors (GluAs)-MPR competitive peptides MPR(DD) and MPR(AA). The MPR(DD) peptide is derived from GluA1 MPR and was previously shown to impair synaptic plasticity and to inhibit GluA1 containing AMPAR insertion into the synapse in an activity-dependent manner. The MPR(AA) peptide is derived from GluA2/4 MPR, and this receptor fragment was shown to be essential for GluA4 protein interaction needed for its insertion into the neuronal membrane and synapse. The peptides were linked to a TAT peptide (TAT-MPR(DD) and TAT-MPR(AA)) to facilitate internalization into LA cells. Infusion of the TAT-MPR(DD) peptide into LA 30 min before fear conditioning led to a significant impairment of long-term fear memory formation. Injection of TAT-MPR(DD) peptide into LA 30 min before fear conditioning impaired short-term fear memory formation. The TAT-MPR(DD) peptide had no effect on memory retrieval when injected into LA 30 min before fear memory test. Infusion of the TAT-MPR(AA) peptide into LA 30 min before fear conditioning led to a significant impairment of long-term fear memory formation. In contrast, the TAT-MPR(AA) had no effect on short-term fear memory formation. A TAT-control peptide had no effect on short- or long-term fear memory. These results show that the AMPAR-MPR in LA is needed for fear memory formation and that the MPR region of GluA1 is essential for acquisition of memory, whereas the MPR region of GluA4 is essential for long-term fear memory consolidation.
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