ArticleMolecular and cellular neurosciences2011
Loss of Thr286 phosphorylation disrupts synaptic CaMKIIα targeting, NMDAR activity and behavior in pre-adolescent mice.
Article in Molecular and cellular neurosciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
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- Quantitative proteomics of dorsolateral prefrontal cortex reveals an early pattern of synaptic dysmaturation in children with idiopathic autism.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Spinophilin-dependent regulation of GluN2B-containing NMDAR-dependent calcium influx, GluN2B surface expression, and cleaved caspase expression.Synapse (New York, N.Y.) · 2023Article
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Reduced exploratory behavior in neuronal nucleoredoxin knockout mice.Redox biology · 2021Article
- The Calcium/Calmodulin-Dependent Kinases II and IV as Therapeutic Targets in Neurodegenerative and Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- Behavioral and Neuroanatomical Consequences of Cell-Type Specific Loss of Dopamine D2 Receptors in the Mouse Cerebral Cortex.Frontiers in behavioral neuroscience · 2021Article
- Enduring alterations in hippocampal astrocytesynaptic proximity following adolescent alcohol exposure: reversal by gabapentin.Neural regeneration research · 2020Article
- Neuronal L-Type Calcium Channel Signaling to the Nucleus Requires a Novel CaMKIIα-Shank3 Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- SK Channel Modulates Synaptic Plasticity by Tuning CaMKIIα/β Dynamics.Frontiers in synaptic neuroscience · 2019Article
- Intracellular emetic signaling cascades by which the selective neurokinin type 1 receptor (NKNeurochemistry international · 2019Article
- Role of Striatal Direct Pathway 2-Arachidonoylglycerol Signaling in Sociability and Repetitive Behavior.Biological psychiatry · 2018Article
- The CaMKII/NMDA receptor complex controls hippocampal synaptic transmission by kinase-dependent and independent mechanisms.Nature communications · 2018Article
- Article
- Proteomic Analysis of Postsynaptic Protein Complexes Underlying Neuronal Plasticity.ACS chemical neuroscience · 2017Review
- Chronic intermittent alcohol disrupts the GluN2B-associated proteome and specifically regulates group I mGlu receptor-dependent long-term depression.Addiction biology · 2017Article
- A Novel HumanThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Mechanisms and Consequences of Dopamine Depletion-Induced Attenuation of the Spinophilin/Neurofilament Medium Interaction.Neural plasticity · 2017Article
- Changes in the Adult GluN2B Associated Proteome following Adolescent Intermittent Ethanol Exposure.PloS one · 2016Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
In order to provide insight into in vivo roles of CaMKIIα autophosphorylation at Thr286 during postnatal development, behavioral, biochemical, and electrophysiological phenotypes of pre-adolescent Thr286 to Ala CaMKIIα knock-in (T286A-KI) and WT mice were examined. T286A-KI mice displayed cognitive deficits in a novel object recognition test and an anxiolytic phenotype in the elevated plus maze, suggesting disruption of normal developmental processes. At the molecular level, the ratio of total CaMKIIα to CaMKIIβ in hippocampal lysates was significantly decreased≈2-fold in T286A-KI mice, and levels of both isoforms in synaptic subcellular fractions were decreased by≈80%. Total levels of GluA1 AMPA-glutamate receptor subunits and phosphorylation of GluA1 at the CaMKII site (Ser831) in synaptic fractions were unaltered, as were the frequency and amplitude of AMPAR-mediated spontaneous excitatory postsynaptic currents at hippocampal CA3-CA1 synapses. Synaptic levels of NMDA-glutamate receptor GluN1, GluN2A and GluN2B subunits also were unaltered. However, the reduced ratio of CaMKII to NMDAR subunits in synaptic fractions was linked to increased synaptic NMDAR-mediated currents in T286A-KI mice, apparently due to increased functional contributions by GluN2B NMDARs (assessed by Ro 25-6981 sensitivity). Thus, disruption of CaMKII synaptic targeting caused by elimination of Thr286 autophosphorylation leads to synaptic and behavioral deficits during pre-adolescence.
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