ArticleNeuroscience2008
Protein kinase C-dependent and independent signaling pathways regulate synaptic GluR1 and GluR4 AMPAR subunits during in vitro classical conditioning.
Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Synaptic Mechanisms of Delay Eyeblink Classical Conditioning: AMPAR Trafficking and Gene Regulation in an In Vitro Model.Molecular neurobiology · 2023Review
- Reactive Oxygen Species Modulate Activity-Dependent AMPA Receptor Transport inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- A brain proteomic investigation of rapamycin effects in theMolecular autism · 2017Article
- Coincidence detection in a neural correlate of classical conditioning is initiated by bidirectional 3-phosphoinositide-dependent kinase-1 signalling and modulated by adenosine receptors.The Journal of physiology · 2015Article
- Sequential delivery of synaptic GluA1- and GluA4-containing AMPA receptors (AMPARs) by SAP97 anchored protein complexes in classical conditioning.The Journal of biological chemistry · 2014Article
- Pain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Article
- Two-stage AMPA receptor trafficking in classical conditioning and selective role for glutamate receptor subunit 4 (tGluA4) flop splice variant.Journal of neurophysiology · 2012Article
- Rapid enrichment of presynaptic protein in boutons undergoing classical conditioning is mediated by brain-derived neurotrophic factor.Neuroscience · 2012Article
- Cloning and characterization of glutamate receptor subunit 4 (GLUA4) and its alternatively spliced isoforms in turtle brain.Journal of molecular neuroscience : MN · 2011Article
- Protein kinase C phosphorylates the cAMP response element binding protein in the hypothalamic paraventricular nucleus during morphine withdrawal.British journal of pharmacology · 2011Article
- Striatal signal transduction and drug addiction.Frontiers in neuroanatomy · 2011Article
- Modeling signal transduction in classical conditioning with network motifs.Frontiers in molecular neuroscience · 2011Article
- Oligomeric amyloid-{beta} inhibits the proteolytic conversion of brain-derived neurotrophic factor (BDNF), AMPA receptor trafficking, and classical conditioning.The Journal of biological chemistry · 2010Article
- AMPA receptor trafficking and learning.The European journal of neuroscience · 2010Review
- Cleavage of proBDNF to BDNF by a tolloid-like metalloproteinase is required for acquisition of in vitro eyeblink classical conditioning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- PKA has a critical role in synaptic delivery of GluR1- and GluR4-containing AMPARs during initial stages of acquisition of in vitro classical conditioning.Journal of neurophysiology · 2009Article
- BDNF-induced synaptic delivery of AMPAR subunits is differentially dependent on NMDA receptors and requires ERK.Neurobiology of learning and memory · 2009Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Protein kinase C (PKC) signal transduction pathways have been implicated in mechanisms of synaptic plasticity and learning, however, the roles of the different PKC family isoforms remain to be clarified. Previous studies showed that NMDAR-mediated trafficking of GluR4-containing AMPARs supports conditioning and that the mitogen-activated protein kinases (MAPKs) have a central role in the synaptic delivery of GluR4 subunits. Here, an in vitro model of classical conditioning in pond turtles, Pseudemys scripta elegans, was used to assess the role of PKC isoforms in mechanisms underlying this form of learning. We show that the PKC antagonists chelerythrine and bisindolylmaleimide I attenuated conditioned response (CR) acquisition and expression, as did the PKCzeta pseudosubstrate peptide inhibitor ZIP. Analysis of protein expression revealed that PKCzeta is activated in early stages of conditioning followed shortly afterward by increased levels of PKCalpha/beta and activation of ERK MAPK. Data also suggest that PKCzeta is upstream from and activates ERK. Finally, protein localization studies using confocal imaging indicate that inhibitors of ERK, but not PKC, suppress colocalization of GluR1 with synaptophysin while inhibitors of PKC and ERK attenuate colocalization of GluR4 with synaptophysin. Together, these data suggest that acquisition of conditioning proceeds by two stages of AMPAR trafficking. The first is PKC-independent and ERK-dependent synaptic delivery of GluR1 subunits to activate silent synapses. This is followed by PKC-dependent and ERK-dependent synthesis and delivery of GluR4 subunits that supports the acquisition of CRs. Therefore, there is a selective role for PKC and MAPK signaling pathways in multistep AMPAR trafficking that mediates acquisition of classical conditioning.
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