ArticleNeurobiology of disease2010
Differential NMDA receptor-dependent calcium loading and mitochondrial dysfunction in CA1 vs. CA3 hippocampal neurons.
Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 71 citations in OpenAlex.
- Sex-Divergent Patterns in Hippocampal and Cortical NMDA Receptor Density Across the Alzheimer's Disease Continuum.International journal of molecular sciences · 2026Article
- Distinct spatial associations of adversity with hippocampal macro- and microstructure in early adolescence.bioRxiv : the preprint server for biology · 2026Article
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- Neuroprotective effects of α-lipoic acid on ischemia/reperfusion injury in global cerebral ischemia mouse model.Scientific reports · 2025Article
- Lithium mitigates hippocampal tau pathology in a rodent model of traumatic brain injury.Acta neuropathologica communications · 2025Article
- How to Pick a Neuroprotective Drug in Stroke Without Losing Your Mind?Life (Basel, Switzerland) · 2025Review
- Transient forebrain ischemia under hyperthermic condition accelerates memory impairment and neuronal death in the gerbil hippocampus by increasing NMDAR1 expression.Molecular medicine reports · 2021Article
- Hippocampal alterations in glutamatergic signaling during amyloid progression in AβPP/PS1 mice.Scientific reports · 2020Article
- Neurodegenerative Diseases - Is Metabolic Deficiency the Root Cause?Frontiers in neuroscience · 2020Review
- Investigating the energy crisis in Alzheimer disease using transcriptome study.Scientific reports · 2019Article
- Maladaptive Downregulation of Autonomous Subthalamic Nucleus Activity following the Loss of Midbrain Dopamine Neurons.Cell reports · 2019Article
- Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways.Frontiers in neurology · 2018Article
- Differences in Reperfusion-Induced Mitochondrial Oxidative Stress and Cell Death Between Hippocampal CA1 and CA3 Subfields Are Due to the Mitochondrial Thioredoxin System.Antioxidants & redox signaling · 2017Article
- Optimized Model of Cerebral IschemiaFrontiers in neuroscience · 2017Article
- Scaffolding protein Homer1a protects against NMDA-induced neuronal injury.Cell death & disease · 2015Article
- Article
- Effects of high-fat diet on neuronal damage, gliosis, inflammatory process and oxidative stress in the hippocampus induced by transient cerebral ischemia.Neurochemical research · 2014Article
- Expression of Nampt in hippocampal and cortical excitatory neurons is critical for cognitive function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Non-specific inhibition of ischemia- and acidosis-induced intracellular calcium elevations and membrane currents by α-phenyl-N-tert-butylnitrone, butylated hydroxytoluene and trolox.International journal of molecular sciences · 2014Article
- Hippocampal sclerosis in dementia, epilepsy, and ischemic injury: differential vulnerability of hippocampal subfields.Journal of neuropathology and experimental neurology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Hippocampal CA1 pyramidal neurons are selectively vulnerable to ischemia, while adjacent CA3 neurons are relatively resistant. Although glutamate receptor-mediated mitochondrial Ca(2+) overload and dysfunction is a major component of ischemia-induced neuronal death, no direct relationship between selective neuronal vulnerability and mitochondrial dysfunction has been demonstrated in intact brain preparations. Here, we show that in organotypic slice cultures NMDA induces much larger Ca(2+) elevations in vulnerable CA1 neurons than in resistant CA3. Consequently, CA1 mitochondria exhibit stronger calcium accumulation, more extensive swelling and damage, stronger depolarization of their membrane potential, and a significant increase in ROS generation. NMDA-induced Ca(2+) and ROS elevations were abolished in Ca(2+)-free medium or by NMDAR antagonists, but not by zinc chelation. We conclude that Ca(2)(+) overload-dependent mitochondrial dysfunction is a determining factor in the selective vulnerability of CA1 neurons.
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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.