ArticleBMC neuroscience2009
Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death.
Article in BMC neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 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
9 citing papers in PubMed, 19 citations in OpenAlex.
- Retraction Note to: Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death.BMC neuroscience · 2017Article
- PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling.Cell death and differentiation · 2015Article
- AMPK Plays a Dual Role in Regulation of CREB/BDNF Pathway in Mouse Primary Hippocampal Cells.Journal of molecular neuroscience : MN · 2015Article
- Implications of glial nitric oxide in neurodegenerative diseases.Frontiers in cellular neuroscience · 2015Review
- Lithium and the other mood stabilizers effective in bipolar disorder target the rat brain arachidonic acid cascade.ACS chemical neuroscience · 2014Review
- [Not Available].EXCLI journal · 2013Article
- Upregulated expression of brain enzymatic markers of arachidonic and docosahexaenoic acid metabolism in a rat model of the metabolic syndrome.BMC neuroscience · 2012Article
- Temporal dependence of cysteine protease activation following excitotoxic hippocampal injury.Neuroscience · 2012Article
- Neuroinflammation and synaptic loss.Neurochemical research · 2012Review
Corrections and comments
- Retraction · 2017-05-09Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · Jagadeesh S Rao has NIH finding of misconduct.
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic N-Methyl-d-aspartate (NMDA) administration to rats is reported to increase arachidonic acid signaling and upregulate neuroinflammatory markers in rat brain. These changes may damage brain cells. In this study, we determined if chronic NMDA administration (25 mg/kg i.p., 21 days) to rats would alter expression of pro- and anti-apoptotic factors in frontal cortex, compared with vehicle control.
resultsUsing real time RT-PCR and Western blotting, chronic NMDA administration was shown to decrease mRNA and protein levels of anti-apoptotic markers Bcl-2 and BDNF, and of their transcription factor phospho-CREB in the cortex. Expression of pro-apoptotic Bax, Bad, and 14-3-3zeta was increased, as well as Fluoro-Jade B (FJB) staining, a marker of neuronal loss.
conclusionThis alteration in the balance between pro- and anti-apoptotic factors by chronic NMDA receptor activation in this animal model may contribute to neuronal loss, and further suggests that the model can be used to examine multiple processes involved in excitotoxicity.
Indexed as
Identifiers
What 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.