ArticlePhysiological research2021
The critical role of hippocampal dopamine in the pathogenesis of hepatic encephalopathy.
Article in Physiological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Gallic acid alleviates hippocampus and cerebellum injuries in a rat model of hepatic encephalopathy.Scientific reports · 2025Article
- Research progress on the roles of dopamine and dopamine receptors in digestive system diseases.Journal of cellular and molecular medicine · 2024Review
- Hepatic encephalopathy.Nature reviews. Disease primers · 2022Review
- Hepatic Encephalopathy and Melatonin.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
6 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of hepatic encephalopathy (HE) has been generally linked to blood ammonia, gamma-aminobutyric acid and serotonin. However, the exact mechanism remains unclear. In the present study, we aimed to explore the role of hippocampal dopamine (DA) and its receptors in the pathogenesis of HE through the use of behavioral testing, western blotting, and immunofluorescence staining in normal rats, HE model rats and rats treated with the DA precursor-levodopa (L-DOPA). HE model rats manifested fibrotic livers and showed serious behavioral disorders. They also had significantly lower hippocampal DA content and increased expression of both D1 and D2 receptors relative to normal rats. After treatment with L-DOPA, the HE model rats showed normal behavior and expression of D1 returned to normal levels. Furthermore, pretreatment with the D1 antagonist SCH23390 blocked the therapeutic effect of L-DOPA on behavior in HE model rats. Taken together, these results clarify that the decrease in hippocampal DA plays a role in the pathogenesis of HE and that this effect is mediated by D1. These findings provide new evidence for the pathogenesis of HE.
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