ArticleNeurotoxicity research2003
Corticosterone down-regulates dopamine D4 receptor in a mouse cerebral cortex neuronal cell line.
Article in Neurotoxicity research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Novel mechanisms and approaches in the study of neurodegeneration and neuroprotection. a review.Neurotoxicity research · 2003Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously reported that restraint stress applied to the gestant mother results in long-lasting effects in the offspring that show an increase in the number of dopamine D2-type receptors in limbic areas on the adult rat brain cortex. Evidence that stress during pregnancy results in activation of the hypothalamic-pituitary-adrenal (HPA) axis has been extensively demonstrated. Therefore, high levels of corticosterone secreted in response to stress by the gestant mother might be one of the predisposing factors for the changes observed in dopamine receptors in the adult rat brain. In this study we addressed the question whether corticosterone would directly up-regulate D2-type receptors in vitro. We have investigated the effect of different concentrations of corticosterone on D4 dopamine receptor in immortalized cell lines from cerebral cortex of normal mouse fetuses, detected by immunocytochemistry employing polyclonal antibodies generated against synthetic peptides homologous to an extracellular domain of D4 receptor. The results show that corticosterone in vitro decreases the number of dopamine D4 receptors, suggesting that the increase of D2-type receptors in adult rats following prenatal stress is not related to a direct action of corticosterone on receptor expression.
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Registered trials
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