ArticleBiological psychiatry2007
Chronic carbamazepine administration reduces N-methyl-D-aspartate receptor-initiated signaling via arachidonic acid in rat brain.
Article in Biological psychiatry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Complex Combination Pharmacotherapy for Bipolar Disorder: Knowing When Less Is More or More Is Better.Focus (American Psychiatric Publishing) · 2019Review
- Psychotropic Drugs for the Management of Chronic Pain and Itch.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Lithium and the other mood stabilizers effective in bipolar disorder target the rat brain arachidonic acid cascade.ACS chemical neuroscience · 2014Review
- Cuneus and fusiform cortices thickness is reduced in trigeminal neuralgia.The journal of headache and pain · 2014Article
- Aging is associated with altered inflammatory, arachidonic acid cascade, and synaptic markers, influenced by epigenetic modifications, in the human frontal cortex.Journal of neurochemistry · 2013Article
- Lamotrigine blocks NMDA receptor-initiated arachidonic acid signalling in rat brain: implications for its efficacy in bipolar disorder.The international journal of neuropsychopharmacology · 2012Article
- Effects of chronic clozapine administration on markers of arachidonic acid cascade and synaptic integrity in rat brain.Psychopharmacology · 2012Article
- Imaging brain signal transduction and metabolism via arachidonic and docosahexaenoic acid in animals and humans.Brain research bulletin · 2012Review
- RETRACTED: Dysregulated glutamate and dopamine transporters in postmortem frontal cortex from bipolar and schizophrenic patients.Journal of affective disorders · 2012Article
- Chronic valproate treatment blocks D2-like receptor-mediated brain signaling via arachidonic acid in rats.Neuropharmacology · 2011Article
- Altered arachidonic acid cascade enzymes in postmortem brain from bipolar disorder patients.Molecular psychiatry · 2011Article
- Extracellular-derived calcium does not initiate in vivo neurotransmission involving docosahexaenoic acid.Journal of lipid research · 2010Article
- Increased excitotoxicity and neuroinflammatory markers in postmortem frontal cortex from bipolar disorder patients.Molecular psychiatry · 2010Article
- Bipolar disorder and mechanisms of action of mood stabilizers.Brain research reviews · 2009Review
- Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death.BMC neuroscience · 2009Article
- Intracellular- and extracellular-derived Ca(2+) influence phospholipase A(2)-mediated fatty acid release from brain phospholipids.Biochimica et biophysica acta · 2009Review
- Imaging elevated brain arachidonic acid signaling in unanesthetized serotonin transporter (5-HTT)-deficient mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009Article
- Mood-stabilizers target the brain arachidonic acid cascade.Current molecular pharmacology · 2009Review
- Chronic administration of valproic acid reduces brain NMDA signaling via arachidonic acid in unanesthetized rats.Neurochemical research · 2008Article
- Chronic NMDA administration increases neuroinflammatory markers in rat frontal cortex: cross-talk between excitotoxicity and neuroinflammation.Neurochemical research · 2008Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLithium and carbamazepine (CBZ) are used to treat mania in bipolar disorder. When given chronically to rats, both agents reduce arachidonic acid (AA) turnover in brain phospholipids and downstream AA metabolism. Lithium in rats also attenuates brain N-methyl-D-aspartic acid receptor (NMDAR) signaling via AA. We hypothesized that, like chronic lithium, chronic CBZ administration to rats would reduce NMDAR-mediated signaling via AA.
methodsWe used our fatty acid method with quantitative autoradiography to image the regional brain incorporation coefficient k* of AA, a marker of AA signaling, in unanesthetized rats that had been given 25 mg/kg/day I.P. CBZ or vehicle for 30 days, then injected with NMDA (25 mg/kg I.P.) or saline. We also measured brain concentrations of two AA metabolites, prostaglandin E(2) (PGE(2)) and thromboxane B(2) (TXB(2)).
resultsIn chronic vehicle-treated rats, NMDA compared with saline increased k* significantly in 69 of 82 brain regions examined, but did not change k* significantly in any region in CBZ-treated rats. In vehicle- but not CBZ-treated rats, NMDA also increased brain concentrations of PGE(2) and TXB(2).
conclusionsChronic CBZ administration to rats blocks increments in the AA signal k*, and in PGE(2) and TXB(2) concentrations that are produced by NMDA in vehicle-treated rats. The clinical action of antimanic drugs might involve inhibition of brain NMDAR-mediated signaling involving AA and its metabolites.
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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.