ArticleToxicologic pathology2011
An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons.
Article in Toxicologic pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting the mitochondrial permeability transition pore for neuroprotection in a piglet model of neonatal hypoxic-ischemic encephalopathy.Journal of neuroscience research · 2021Article
- Chronic Intermittent Mild Whole-Body Hypothermia Is Therapeutic in a Mouse Model of ALS.Cells · 2021Article
- Skeletal Muscle-Restricted Expression of Human SOD1 in Transgenic Mice Causes a Fatal ALS-Like Syndrome.Frontiers in neurology · 2020Article
- DNA Damage Response and Repair, DNA Methylation, and Cell Death in Human Neurons and Experimental Animal Neurons Are Different.Journal of neuropathology and experimental neurology · 2018Article
- Effect of caffeic acid phenethyl ester on oxidant and anti-oxidant status of liver and serum in a rat model with acute methanol intoxication.Irish journal of medical science · 2017Article
- Enforced DNA repair enzymes rescue neurons from apoptosis induced by target deprivation and axotomy in mouse models of neurodegeneration.Mechanisms of ageing and development · 2017Article
- Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies.Neural plasticity · 2016Review
- Modelling the molecular mechanism of protein-protein interactions and their inhibition: CypD-p53 case study.Molecular diversity · 2015Article
- Sex differences in mitochondrial (dys)function: Implications for neuroprotection.Journal of bioenergetics and biomembranes · 2015Review
- Mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice.Neurobiology of aging · 2014Article
- Inhibition of cyclophilin D by cyclosporin A promotes retinal ganglion cell survival by preventing mitochondrial alteration in ischemic injury.Cell death & disease · 2014Article
- Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.Molecular neurobiology · 2012Review
- Biology of mitochondria in neurodegenerative diseases.Progress in molecular biology and translational science · 2012Review
- Many stimuli pull the necrotic trigger, an overview.Cell death and differentiation · 2012Review
- Epigenetic regulation of motor neuron cell death through DNA methylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Generation and characterization of transgenic mice expressing mitochondrial targeted red fluorescent protein selectively in neurons: modeling mitochondriopathy in excitotoxicity and amyotrophic lateral sclerosis.Molecular neurodegeneration · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Researchers used transgenic mice expressing enhanced-green fluorescent protein (eGFP) driven by either the glycine transporter-2 gene promoter to specifically visualize glycinergic interneurons or the homeobox-9 (Hb9) gene promoter to visualize motoneurons for assessing their vulnerabilities to excitotoxins in vivo. Stereotaxic excitotoxic lesions were made in adult male and female mouse lumbar spinal cord with the specific N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid (QA) and the non-NMDA ion channel glutamate receptor agonist kainic acid (KA). QA and KA induced large-scale degeneration of glycinergic interneurons in spinal cord. Glycinergic interneurons were more sensitive than motoneurons to NMDA receptor-mediated and non-NMDA glutamate receptor-mediated excitotoxicity. Outcome after spinal cord excitotoxicity was gender-dependent, with males showing greater sensitivity than females. Excitotoxic degeneration of spinal interneurons resembled apoptosis, while motoneuron degeneration appeared non-apoptotic. Perikaryal mitochondrial accumulation was antecedent to both NMDA and non-NMDA receptor-mediated excitotoxic stimulation of interneurons and motoneurons. Genetic ablation of cyclophilin D, a regulator of the mitochondrial permeability transition pore (mPTP), protected both interneurons and motoneurons from excitotoxicity. The results demonstrate in adult mouse spinal cord that glycinergic interneurons are more sensitive than motoneurons to excitotoxicity that stimulates mitochondrial accumulation, and that the mPTP has pro-death functions mediating apoptotic and non-apoptotic neuronal degeneration in vivo.
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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.