ArticleThe Journal of comparative neurology2009
Drebrin a knockout eliminates the rapid form of homeostatic synaptic plasticity at excitatory synapses of intact adult cerebral cortex.
Article in The Journal of comparative neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Functional Differences Between Neuronal and Non-neuronal Isoforms of Drebrin.Journal of molecular biology · 2025Article
- Ketamine ameliorates activity-based anorexia of adolescent female mice through changes in GluN2B-containing NMDA receptors at postsynaptic cytoplasmic locations of pyramidal neurons and interneurons of medial prefrontal cortex.Brain structure & function · 2024Article
- Anatomical and molecular development of the human primary visual cortex.Frontiers in cellular neuroscience · 2024Review
- Individual differences in the positive outcome from adolescent ketamine treatment in a female mouse model of anorexia nervosa involve drebrin A at excitatory synapses of the medial prefrontal cortex.Synapse (New York, N.Y.) · 2023Article
- Pathway-specific GABAergic inhibition contributes to the gain of resilience against anorexia-like behavior of adolescent female mice.Frontiers in behavioral neuroscience · 2022Article
- Interplay Between Human Gut BacteriaFrontiers in immunology · 2020Article
- NR2A- and NR2B-NMDA receptors and drebrin within postsynaptic spines of the hippocampus correlate with hunger-evoked exercise.Brain structure & function · 2017Article
- Investigation of hippocampal synaptic transmission and plasticity in mice deficient in the actin-binding protein Drebrin.Scientific reports · 2017Article
- Drebrin and Spermatogenesis.Advances in experimental medicine and biology · 2017Article
- Review
- Methadone Reverses Analgesic Tolerance Induced by Morphine Pretreatment.The international journal of neuropsychopharmacology · 2016Article
- The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Drebrin contains a cryptic F-actin-bundling activity regulated by Cdk5 phosphorylation.The Journal of cell biology · 2013Article
- Presenilin conditional double knockout mice exhibit decreases in drebrin a at hippocampal CA1 synapses.Synapse (New York, N.Y.) · 2012Article
- Epigenetic modifications in frontal cortex from Alzheimer's disease and bipolar disorder patients.Translational psychiatry · 2012Article
- Heterogeneous reallocation of presynaptic efficacy in recurrent excitatory circuits adapting to inactivity.Nature neuroscience · 2011Article
- Disturbed neurotransmitter transporter expression in Alzheimer's disease brain.Journal of Alzheimer's disease : JAD · 2011Article
- Neuroplasticity of the central hypercapnic ventilatory response: teratogen-induced impairment and subsequent recovery during development.Developmental neurobiology · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Homeostatic synaptic plasticity (HSP) is important for maintaining neurons' excitability within the dynamic range and for protecting neurons from unconstrained long-term potentiation that can cause breakdown of synapse specificity (Turrigiano [2008] Cell 135:422-435). Knowledge of the molecular mechanism underlying this phenomenon remains incomplete, especially for the rapid form of HSP. To test whether HSP in adulthood depends on an F-actin binding protein, drebrin A, mice deleted of the adult isoform of drebrin (DAKO) but retaining the embryonic isoform (drebrin E) were generated. HSP was assayed by determining whether the NR2A subunit of N-methyl-D-aspartate receptors (NMDARs) can rise rapidly within spines following the application of an NMDAR antagonist, D-APV, onto the cortical surface. Electron microscopic immunocytochemistry revealed that, as expected, the D-APV treatment of wild-type (WT) mouse cortex increased the proportion of NR2A-immunolabeled spines within 30 minutes relative to basal levels in hemispheres treated with an inactive enantiomer, L-APV. This difference was significant at the postsynaptic membrane and postsynaptic density (i.e., synaptic junction) as well as at nonsynaptic sites within spines and was not accompanied by spine size changes. In contrast, the D-APV treatment of DAKO brains did not augment NR2A labeling within the spine cytoplasm or at the synaptic junction, even though basal levels of NR2A were not significantly different from those of WT cortices. These findings indicate that drebrin A is required for the rapid (<30 minutes) form of HSP at excitatory synapses of adult cortices, whereas drebrin E is sufficient for maintaining basal NR2A levels within spines.
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