ReviewMolecular neurobiology2005
Kainic acid-mediated excitotoxicity as a model for neurodegeneration.
Review in Molecular neurobiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
What it found
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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.
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.
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Who cites it
154 citing papers in PubMed, 361 citations in OpenAlex.
- 3-Nitropropionic Acid-Induced Huntington's Disease in Preclinical Models: Mechanisms, Peripheral Toxicities, Model Gaps, and Future Directions.Molecular neurobiology · 2026Review
- Microfluidic co-culture system for synaptically segregated neural networks to explore astrocyte-driven neural pathology.Microsystems & nanoengineering · 2026Article
- Acute hyperexcitability differentially affects hippocampal neurogenesis features and spatial memory.Frontiers in cellular neuroscience · 2026Article
- Effects of Troxerutin on Oxidative Stress, Inflammation and Galectin- 3 Expression in Intracerebroventricular Kainic Acid-Induced Neurotoxicity.Inflammation · 2025Article
- Stra8 links neuronal activity to inhibitory circuit protection in the adult mouse brain.Cell reports · 2025Article
- Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.Molecular neurobiology · 2025Review
- KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.Frontiers in molecular neuroscience · 2025Article
- Xanthohumol Protects Against Neuronal Excitotoxicity and Mitochondrial Dysfunction in APP/PS1 Mice: An Omics-Based Study.Nutrients · 2024Article
- How is Excitotoxicity Being Modelled in iPSC-Derived Neurons?Neurotoxicity research · 2024Review
- Sodium Houttuyfonate Prevents Seizures and Neuronal Cell Loss by Maintaining Glutamatergic System Stability in Male Rats with Kainic Acid-Induced Seizures.Biomedicines · 2024Article
- Gypenoside XVII Reduces Synaptic Glutamate Release and Protects against Excitotoxic Injury in Rats.Biomolecules · 2024Article
- Micro-and mesoscale aspects of neurodegeneration in engineered human neural networks carrying the LRRK2 G2019S mutation.Frontiers in cellular neuroscience · 2024Article
- The extract based on the Kampo formula daikenchuto (Da Jian Zhong Tang) induces Bdnf expression and has neurotrophic effects in cultured cortical neurons.Journal of natural medicines · 2023Article
- Heat shock factor HSF1 regulates BDNF gene promoters upon acute stress in the hippocampus, together with pCREB.Journal of neurochemistry · 2023Article
- Review
- Riluzole and novel naphthalenyl substituted aminothiazole derivatives prevent acute neural excitotoxic injury in a rat model of temporal lobe epilepsy.Neuropharmacology · 2023Article
- Role of microRNA-34b-5p in cancer and injury: how does it work?Cancer cell international · 2022Review
- Inhibition of Synaptic Glutamate Exocytosis and Prevention of Glutamate Neurotoxicity by Eupatilin fromInternational journal of molecular sciences · 2022Article
- Article
- The autophagy inducer SMER28 attenuates microtubule dynamics mediating neuroprotection.Scientific reports · 2022Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal excitation involving the excitatory glutamate receptors is recognized as an important underlying mechanism in neurodegenerative disorders. Excitation resulting from stimulation of the ionotropic glutamate receptors is known to cause the increase in intracellular calcium and trigger calcium-dependent pathways that lead to neuronal apoptosis. Kainic acid (KA) is an agonist for a subtype of ionotropic glutamate receptor, and administration of KA has been shown to increase production of reactive oxygen species, mitochondrial dysfunction, and apoptosis in neurons in many regions of the brain, particularly in the hippocampal subregions of CA1 and CA3, and in the hilus of dentate gyrus (DG). Systemic injection of KA to rats also results in activation of glial cells and inflammatory responses typically found in neurodegenerative diseases. KA-induced selective vulnerability in the hippocampal neurons is related to the distribution and selective susceptibility of the AMPA/kainate receptors in the brain. Recent studies have demonstrated ability of KA to alter a number of intracellular activities, including accumulation of lipofuscin-like substances, induction of complement proteins, processing of amyloid precursor protein, and alteration of tau protein expression. These studies suggest that KA-induced excitotoxicity can be used as a model for elucidating mechanisms underlying oxidative stress and inflammation in neurodegenerative diseases. The focus of this review is to summarize studies demonstrating KA-induced excitotoxicity in the central nervous system and possible intervention by anti-oxidants.
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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.