ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Mechanisms and effects of intracellular calcium buffering on neuronal survival in organotypic hippocampal cultures exposed to anoxia/aglycemia or to excitotoxins.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 130 citations in OpenAlex.
- Clinical pharmacology of DP-b99 in healthy volunteers: first administration to humans.British journal of clinical pharmacology · 2005Trial
- Computational analysis of cortical neuronal excitotoxicity in a large animal model of neonatal brain injury.Journal of neurodevelopmental disorders · 2022Article
- BAPTA, a calcium chelator, neuroprotects injured neurons in vitro and promotes motor recovery after spinal cord transection in vivo.CNS neuroscience & therapeutics · 2021Article
- Identification of Multi-Target Anti-AD Chemical Constituents From Traditional Chinese Medicine Formulae by Integrating Virtual Screening andFrontiers in pharmacology · 2021Article
- Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures.Neurotoxicity research · 2018Article
- Altered Synaptic Vesicle Release and CaFrontiers in molecular neuroscience · 2018Article
- Two-photon deep-tissue spatially resolved mitochondrial imaging using membrane potential fluorescence fluctuations.Biomedical optics express · 2018Article
- Article
- Organotypic Hippocampal Slices as Models for Stroke and Traumatic Brain Injury.Molecular neurobiology · 2016Review
- Marine compound xyloketal B reduces neonatal hypoxic-ischemic brain injury.Marine drugs · 2014Article
- Low pH environmental stress inhibits LPS and LTA-stimulated proinflammatory cytokine production in rat alveolar macrophages.BioMed research international · 2013Article
- Mitochondrial membrane potential probes and the proton gradient: a practical usage guide.BioTechniques · 2011Review
- Neuroprotective properties of levosimendan in an in vitro model of traumatic brain injury.BMC neurology · 2010Article
- Simulated ischaemia induces Ca2+-independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus.The Journal of physiology · 2010Article
- A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures.Neurochemical research · 2009Article
- Argon: neuroprotection in in vitro models of cerebral ischemia and traumatic brain injury.Critical care (London, England) · 2009Article
- Propofol: neuroprotection in an in vitro model of traumatic brain injury.Critical care (London, England) · 2009Article
- The electrical response of cerebellar Purkinje neurons to simulated ischaemia.Brain : a journal of neurology · 2005Article
- Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Cellular death in hippocampus in response to PI3K pathway inhibition and oxygen and glucose deprivation.Neurochemical research · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal calcium loading attributable to hypoxic/ischemic injury is believed to trigger neurotoxicity. We examined in organotypic hippocampal slice cultures whether artificially and reversibly enhancing the Ca2+ buffering capacity of neurons reduces the neurotoxic sequelae of oxygen-glucose deprivation (OGD), whether such manipulation has neurotoxic potential, and whether the mechanism underlying these effects is pre- or postsynaptic. Neurodegeneration caused over 24 hr by 60 min of OGD was triggered largely by NMDA receptor activation and was attenuated temporarily by pretreating the slices with cell-permeant Ca2+ buffers such as 1, 2 bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid acetoxymethyl ester (BAPTA-AM). This pretreatment produced a transient, reversible increase in intracellular buffer content as demonstrated autoradiographically using slices loaded with 14C-BAPTA-AM and by confocal imaging of slices loaded with the BAPTA-AM analog calcium green-acetoxymethyl ester (AM). The time courses of 14C-BAPTA retention and of neuronal survival after OGD were identical, indicating that increased buffer content is necessary for the observed protective effect. Protection by Ca2+ buffering originated presynaptically because BAPTA-AM was ineffective when endogenous transmitter release was bypassed by directly applying NMDA to the cultures, and because pretreatment with the low Ca2+ affinity buffer 2-aminophenol-N,N,O-triacetic acid acetoxymethyl ester, which attenuates excitatory transmitter release, attenuated neurodegeneration. Thus, in cultured hippocampal slices, enhancing neuronal Ca2+ buffering unequivocally attenuates or delays the onset of anoxic neurodegeneration, likely by attenuating the synaptic release of endogenous excitatory neurotransmitters (excitotoxicity).
Indexed as
Identifiers
9133378PMC6573708W1497472237What OpenQuestion holds
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.