ArticleJournal of neurotrauma2008
Differential hippocampal protection when blocking intracellular sodium and calcium entry during traumatic brain injury in rats.
Article in Journal of neurotrauma, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.Molecular neurobiology · 2025Review
- Upregulation of Na/H Exchanger in Astrogliosis and Early Alzheimer's Disease Pathogenesis.Aging and disease · 2024Article
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- Drug development in targeting ion channels for brain edema.Acta pharmacologica Sinica · 2020Article
- Review
- Dynamin and reverse-mode sodium calcium exchanger blockade confers neuroprotection from diffuse axonal injury.Cell death & disease · 2019Article
- Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration.Journal of neurotrauma · 2019Article
- Pathophysiology and treatment of cerebral edema in traumatic brain injury.Neuropharmacology · 2019Review
- Neuroprotection induced by N-acetylcysteine and selenium against traumatic brain injury-induced apoptosis and calcium entry in hippocampus of rat.Cellular and molecular neurobiology · 2014Article
- Blockage of the upregulation of voltage-gated sodium channel nav1.3 improves outcomes after experimental traumatic brain injury.Journal of neurotrauma · 2014Article
- Loss of Acid sensing ion channel-1a and bicarbonate administration attenuate the severity of traumatic brain injury.PloS one · 2013Article
- The increased activity of TRPV4 channel in the astrocytes of the adult rat hippocampus after cerebral hypoxia/ischemia.PloS one · 2012Article
- Calpains and delayed calcium deregulation in excitotoxicity.Neurochemical research · 2010Article
- Acid-sensing ion channels: A new target for pain and CNS diseases.Current opinion in drug discovery & development · 2009Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
This study investigated the contributions of the reverse mode of the sodium-calcium exchanger (NCX) and the type 1 sodium-proton antiporter (NHE-1) to acute astrocyte and neuronal pathology in the hippocampus following fluid percussion traumatic brain injury (TBI) in the rat. KB-R7943, EIPA, or amiloride, which respectively inhibit NCX, NHE-1, or NCX, NHE-1, and ASIC1a (acid-sensing ion channel type 1a), was infused intraventricularly over a 60-min period immediately prior to TBI. Astrocytes were immunostained for glial fibrillary acidic protein (GFAP), and degenerating neurons were identified by Fluoro-Jade staining at 24 h after injury. Stereological analysis of the CA2/3 sub-regions of the hippocampus demonstrated that higher doses of KB-R7943 (2 and 20 nmoles) significantly reduced astrocyte GFAP immunoreactivity compared to vehicle-treated animals. EIPA (2-200 nmoles) did not alter astrocyte GFAP immunoreactivity. Amiloride (100 nmoles) significantly attenuated the TBI-induced acute reduction in astrocyte GFAP immunoreactivity. Of the three compounds examined, only amiloride (100 nmoles) reduced hippocampal neuronal degeneration assessed with Fluoro-Jade. The results provide additional evidence of acute astrocyte pathology in the hippocampus following TBI, while suggesting that activation of NHE-1 and the reverse mode of NCX contribute to both astrocyte and neuronal pathology following experimental TBI.
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