ArticlePsychopharmacology2012
Chronic treatment with serotonin reuptake inhibitor antidepressant (SSRI) combined with an antipsychotic regulates GABA-A receptor in rat prefrontal cortex.
Article in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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0 citing papers in PubMed, 3 citations in OpenAlex.
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Abstract
introductionThe combination of selective serotonin reuptake inhibitor (SSRI) antidepressants and antipsychotics is currently used for the treatment of negative symptoms of schizophrenia. However, the biochemical mechanism mediating the clinical effectiveness of this treatment remains obscure. Previously, we have reported that acute haloperidol (HALO)-fluvoxamine (FLU) in vivo and in vitro treatment regulated GABA-Aβ2/3 receptor subunits, and protein kinase C (PKC) and mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) signaling pathways.
findingsIn the present study, we demonstrated that chronic HALO-FLU treatment, but not each drug alone, significantly decreased GABA-Aβ2/3 receptor expression (25 ± 6.2% vs. control) and caused receptor translocation from the membrane to the cytosol in rat prefrontal cortex. Phosphorylation of PKC and ERK2 was affected differently by HALO-FLU combination than by the individual drug treatments. HALO and FLU each given alone increased PKC phosphorylation levels (29 ± 15% and 40 ± 11.8%, vs. control, respectively) and did not affect ERK2 phosphorylation, while HALO-FLU combined treatment did not alter PKC phosphorylation levels and significantly decreased ERK2 phosphorylation levels (58 ± 4.4% vs. control). GABA-A receptor downregulation in the brain was accompanied by a decrease in GABA-A function, as shown in muscimol-induced loss of righting reflex (22 ± 9.8 min).
conclusionsWe provide a brief heuristic overview of our preclinical and clinical studies with the SSRI-antipsychotic combination and argue that the finding that it causes similar dynamic changes in laboratory and clinical domains, specifically in GABA-A β2/3 receptor and PKC, strongly supports the hypothesis that the GABA-A receptors and their regulatory systems are involved in the molecular mechanisms underlying the clinical effectiveness of SSRI augmentation.
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