ArticleMolecular neurobiology2016
Kainic Acid-Induced Golgi Complex Fragmentation/Dispersal Shifts the Proteolysis of Reelin in Primary Rat Neuronal Cells: An In Vitro Model of Early Stage Epilepsy.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The Golgi apparatus: adaptations to neuronal shape and functions.The EMBO journal · 2026Review
- The neuronal Golgi in neural circuit formation and reorganization.Frontiers in neural circuits · 2024Review
- H19 silencing decreases kainic acid-induced hippocampus neuron injury via activating the PI3K/AKT pathway via the H19/miR-206 axis.Experimental brain research · 2022Article
- Golgi Complex Dynamics and Its Implication in Prevalent Neurological Disorders.Frontiers in cell and developmental biology · 2019Review
- Trkb-IP3 Pathway Mediating Neuroprotection in Rat Hippocampal Neuronal Cell Culture Following Induction of Kainic Acid.The Malaysian journal of medical sciences : MJMS · 2018Article
- Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases.Molecular neurobiology · 2018Review
- Asymmetric Golgi Repositioning: A Prerequisite for Appropriate Dendrite Formation in Adult-Born Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Repositioning of Somatic Golgi Apparatus Is Essential for the Dendritic Establishment of Adult-Born Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Desacetylvinblastine Monohydrazide Disrupts Tumor Vessels by Promoting VE-cadherin Internalization.Theranostics · 2018Article
- Golgi apparatus dis- and reorganizations studied with the aid of 2-deoxy-D-glucose and visualized by 3D-electron tomography.Histochemistry and cell biology · 2017Article
- Oxytocin modulates GABAScientific reports · 2016Article
- Cyclosporine A Treatment Abrogates Ischemia-Induced Neuronal Cell Death by Preserving Mitochondrial Integrity through Upregulation of the Parkinson's Disease-Associated Protein DJ-1.CNS neuroscience & therapeutics · 2016Article
- A Nuclear Attack on Traumatic Brain Injury: Sequestration of Cell Death in the Nucleus.CNS neuroscience & therapeutics · 2016Article
- Reelin Proteolysis Affects Signaling Related to Normal Synapse Function and Neurodegeneration.Frontiers in cellular neuroscience · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The endoplasmic reticulum-lysosome-Golgi network plays an important role in Reelin glycosylation and its proteolytic processing. Golgi complex fragmentation is associated with the separation of Reelin from this network. Kainic acid (KA) is an excitotoxic agent commonly used to induce epilepsy in rodents. The relationship between KA-induced neuronal damage and Golgi complex fragmentation has not been investigated, leaving a major gap in our understanding of the molecular mechanism underlying the development of pathophysiology in epilepsy. We cultured primary rat cortical neurons eitherin ambient condition (control) or treated with a range of KA doses to reveal whether Golgi complex fragmentation impaired neuronal function. The half-life maximal inhibitory concentration (IC50) value of KA was detected to be approximately 5 μM, whereby at these concentrations, KA impaired neuronal viability, which was closely associated with initial Golgi complex fragmentation and subsequent reduction in both the expression and glycosylation patterns of Reelin. These findings implicate that Golgi complex fragmentation and Reelin dysfunction are key contributors to neuronal cell death in the early stage of epilepsy pathophysiology, thereby representing as novel disease biomarkers, as well as potent therapeutic targets for epilepsy.
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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.