ReviewFrontiers in bioscience (Scholar edition)2009
Calpain and the glutamatergic synapse.
Review in Frontiers in bioscience (Scholar edition), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Proteolytic cleavage of G3BP1 by calpain 1 couples NMDAR activation to mTOR-dependent local translation.EMBO reports · 2026Article
- Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons.iScience · 2025Article
- Systematic review of melatonin in cerebral ischemia-reperfusion injury: critical role and therapeutic opportunities.Frontiers in pharmacology · 2024Review
- In the fast lane: Receptor trafficking during status epilepticus.Epilepsia open · 2023Review
- Calpain signaling: from biology to therapeutic opportunities in neurodegenerative disorders.Frontiers in veterinary science · 2023Review
- The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.Frontiers in synaptic neuroscience · 2022Review
- Calpastatin Overexpression Protects against Excitotoxic Hippocampal Injury and Traumatic Spinal Cord Injury.Journal of neurotrauma · 2020Article
- Calcium-Activated Calpain Specifically Cleaves Glutamate Receptor IIA But Not IIB at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Mitofusin 2 Regulates Axonal Transport of Calpastatin to Prevent Neuromuscular Synaptic Elimination in Skeletal Muscles.Cell metabolism · 2018Article
- Regulatory role of calpain in neuronal death.Neural regeneration research · 2018Review
- Environmental Enrichment Mitigates Deficits after Repetitive Mild Traumatic Brain Injury.Journal of neurotrauma · 2017Article
- Differential role of calpain-dependent protein cleavage in intermediate and long-term operant memory in Aplysia.Neurobiology of learning and memory · 2017Article
- Activity- and development-dependent down-regulation of TARPγ8 and GluA1 in cultured rat hippocampal neurons.Acta pharmacologica Sinica · 2016Article
- K-Cl cotransporter KCC2--a moonlighting protein in excitatory and inhibitory synapse development and function.Pflugers Archiv : European journal of physiology · 2015Review
- MFN2 couples glutamate excitotoxicity and mitochondrial dysfunction in motor neurons.The Journal of biological chemistry · 2015Article
- Article
- Researching glutamate - induced cytotoxicity in different cell lines: a comparative/collective analysis/study.Frontiers in cellular neuroscience · 2015Review
- FRET-FLIM investigation of PSD95-NMDA receptor interaction in dendritic spines; control by calpain, CaMKII and Src family kinase.PloS one · 2014Article
- Conditional disruption of calpain in the CNS alters dendrite morphology, impairs LTP, and promotes neuronal survival following injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Calpain 1 knockdown improves tissue sparing and functional outcomes after spinal cord injury in rats.Journal of neurotrauma · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calpain is a ubiquitous protease found in different tissue types and in many organisms including mammals. It generally does not destroy its large variety of substrates, but more commonly disrupts their function. In neurons, many of its substrates become dysregulated as a result of cleavage of their regulatory domain by this protease, leading to altered signaling between cells. In glutamatergic synaptic transmission, direct targets of calpain include all of the major glutamate receptors: NMDA receptors, AMPA receptors and mGluR. By cleaving these receptors and associated intracellular proteins, calpain may regulate the physiology at glutamatergic synapses. As a result, calpain-mediated cleavage in neurons might not only be involved in pathological events like excitotoxicity, but may also have neuroprotective effects and roles in physiological synaptic transmission.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.