Different effects of five dopamine receptor subtypes on nuclear factor-κB activity in NG108-15 cells and mouse brain

Yusuke Takeuchi, Kohji Fukunaga

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

We previously showed that dopamine receptors D1R and D2R expressed in NG108-15 cells activated protein kinase A and extracellular signal-regulated kinase (ERK) respectively, resulting in differential activation of nuclear factor (NF)-κB activity. To investigate whether other dopamine receptor subtypes regulate NF-κB, we established NG108-15 cells stably expressing D3R, D4R and D5R (NGD3R, NGD4R and NGD5R). D5R stimulation with SKF 38393 decreased NF-κB luciferase reporter activity in NGD5R cells, similar to D1R stimulation in NGD1R cells. However, D3R or D4R stimulation with quinpirole showed no change in NF-κB-Luci activity, although forskolin-induced cyclic AMP responsive element-Luci activation was attenuated by quinpirole treatment in NGD2LR, NGD3R and NGD4R cells. As expected, activation of ERK or serum responsive element-luciferase reporter not observed following stimulation with quinpirole in D3R- or D4R-expressing cells. We further examined the effects of haloperidol and risperidone, which are typical and atypical antipsychotic drugs respectively, on NF-κB activity by gel shift assay in mouse frontal cortex. Haloperidol treatment slightly attenuated basal NF-κB activity. By contrast, risperidone treatment enhanced NF-κB activity. Taken together, D2R and D1R/D5R had opposite effects on NF-κB activity in NG108-15 cells. Risperidone up-regulated and haloperidol down-regulated NF-κB activity in mouse brain. This effect may be related to the atypical antipsychotic properties of risperidone.

Original languageEnglish
Pages (from-to)41-50
Number of pages10
JournalJournal of Neurochemistry
Volume88
Issue number1
DOIs
Publication statusPublished - 2004 Jan

Keywords

  • Dopamine receptor
  • Haloperidol
  • NG108-15 cells
  • Nuclear factor κB
  • Risperidone

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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