ArticleNeurochemical research2008
Chronic carbamazepine administration attenuates dopamine D2-like receptor-initiated signaling via arachidonic acid in rat brain.
Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Narrative Review on Common Traits of Parkinson's Disease and Epilepsy.Journal of clinical medicine · 2025Review
- Trimetazidine, an Anti-Ischemic Drug, Reduces the Antielectroshock Effects of Certain First-Generation Antiepileptic Drugs.International journal of molecular sciences · 2022Article
- Pharmacogenetics of Carbamazepine and Valproate: Focus on Polymorphisms of Drug Metabolizing Enzymes and Transporters.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Complex Combination Pharmacotherapy for Bipolar Disorder: Knowing When Less Is More or More Is Better.Focus (American Psychiatric Publishing) · 2019Review
- Characterization of ST14A Cells for Studying Modulation of Voltage-Gated Calcium Channels.PloS one · 2015Article
- Lithium and the other mood stabilizers effective in bipolar disorder target the rat brain arachidonic acid cascade.ACS chemical neuroscience · 2014Review
- Second messenger/signal transduction pathways in major mood disorders: moving from membrane to mechanism of action, part II: bipolar disorder.CNS spectrums · 2013Review
- 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
- Chronic valproate treatment blocks D2-like receptor-mediated brain signaling via arachidonic acid in rats.Neuropharmacology · 2011Article
- 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
- Decreased GRK3 but not GRK2 expression in frontal cortex from bipolar disorder patients.The international journal of neuropsychopharmacology · 2009Article
- Chronic administration of valproic acid reduces brain NMDA signaling via arachidonic acid in unanesthetized rats.Neurochemical research · 2008Article
- Gabapentin's minimal action on markers of rat brain arachidonic acid metabolism agrees with its inefficacy against bipolar disorder.Prostaglandins, leukotrienes, and essential fatty acidsArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Observations that dopaminergic antagonists are beneficial in bipolar disorder and that dopaminergic agonists can produce mania suggest that bipolar disorder involves excessive dopaminergic transmission. Thus, mood stabilizers used to treat the disease might act in part by downregulating dopaminergic transmission. In agreement, we reported that dopamine D2-like receptor mediated signaling involving arachidonic acid (AA, 20:4n-6) was downregulated in rats chronically treated with lithium. To see whether chronic carbamazepine, another mood stabilizer, did this as well, we injected i.p. saline or the D2-like receptor agonist, quinpirole (1 mg/kg), into unanesthetized rats that had been pretreated for 30 days with i.p. carbamazepine (25 mg/kg/day) or vehicle, and used quantitative autoradiography to measure regional brain incorporation coefficients (k*) for AA, markers of signaling. We also measured brain prostaglandin E2 (PGE2), an AA metabolite. In vehicle-treated rats, quinpirole compared with saline significantly increased k* for AA in 35 of 82 brain regions examined, as well as brain PGE2 concentration. Affected regions belong to dopaminergic circuits and have high D2-like receptor densities. Chronic carbamazepine pretreatment prevented the quinpirole-induced increments in k* and in PGE2. These findings are consistent with the hypothesis that effective mood stabilizers generally downregulate brain AA signaling via D2-like receptors, and that this signaling is upregulated in bipolar disorder.
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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.