Retracted: Chronic NMDA administration to rats up‐regulates frontal cortex cytosolic phospholipase A<sub>2</sub>and its transcription factor, activator protein‐2
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Dossier post-publication
- Nature
- Retraction
- Motif
- Falsification/Fabrication of Data;Investigation by Company/Institution;Misconduct - Official Investigation(s) and/or Finding(s);Misconduct by Author;
- Date
- 2/13/2017 0:00
- Signalé par OpenAlex ?
- Oui
Source : Retraction Watch, jointe par DOI. OpenAlex consigne la rétractation dans is_retracted, un booléen sur un espace d'états à au moins quatre valeurs ; il ne peut donc exprimer ni une expression de préoccupation, ni une correction, ni un rétablissement, et les rapporte comme false, ce qui se lit comme « rien à signaler ».
Résumé
Excessive N-methyl-D-aspartate (NMDA) signaling is thought to contribute to bipolar disorder symptoms. Lithium and carbamazepine, effective against bipolar mania, are reported in rats to reduce brain transcription of an arachidonic acid selective calcium-dependent cytosolic phospholipase A(2) (cPLA(2)), as well as expression of one of its transcription factors, activator protein (AP)-2. In this study, we determined if chronic administration of NMDA (25 mg/kg i.p.) to rats would increase brain cPLA(2) and AP-2 expression, as these antimanic drugs are known to down-regulate excessive NMDA signaling. Administration of a daily subconvulsive dose of NMDA to rats for 21 days decreased frontal cortex NMDA receptor (NR)-1 and NR-3A subunits and increased cPLA(2) activity, phosphorylation, protein, and mRNA levels. The activity and protein levels of secretory phospholipase A(2) or calcium-independent phospholipase A(2) were not changed significantly. Chronic NMDA also increased the DNA-binding activity of AP-2 and the protein levels of its alpha and beta subunits. These changes were absent following acute (3 h earlier) NMDA administration. The changes, opposite to those found following chronic lithium or carbamazepine, are consistent with up-regulated arachidonic acid release due to excessive NR signaling and may be a contributing factor to bipolar mania.
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La notice
- Revue
- Journal of Neurochemistry
- Thématique
- Bipolar Disorder and Treatment
- Domaine
- Medicine
- Établissements canadiens
- University of Toronto
- Organismes subventionnaires
- National Cancer InstituteNational Institutes of Health
- Mots-clés
- NMDA receptorEndocrinologyInternal medicineArachidonic acidPhospholipase A2Activator (genetics)Phospholipase CCytosolChemistryPhospholipase APhospholipaseBiologyReceptorMedicineBiochemistryEnzyme
- Résumé présent dans OpenAlex
- oui