ArticleEndocrine2005
The serotonin type 3A receptor facilitates luteinizing hormone release and LHbeta promoter activity in immortalized pituitary gonadotropes.
Article in Endocrine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Tenets in Microbial Endocrinology: A New Vista in Teleost Reproduction.Frontiers in physiology · 2022Review
- Ion channels and signaling in the pituitary gland.Endocrine reviews · 2010Review
- Follicle stimulating and leutinizing hormones, estradiol and testosterone in Prader-Willi syndrome.American journal of medical genetics. Part A · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The 5-hydroxytryptamine type 3A receptor (5-HT3AR) is a ligand-gated cation channel activated by serotonin. This receptor is expressed throughout the nervous system as well as in the pituitary gland. Although it has been documented that the 5-HT3AR modulates exocytosis in neurons, its role in the pituitary gland has not been determined. Previous research has shown that the 5-HT3AR modulates circulating gonadotropin levels in vivo. It is unclear, however, if its activation in the pituitary gland mediates these effects or if receptors elsewhere in the hypothalamus-pituitary-gondal axis are responsible. To investigate the potential for the 5-HT3AR to modulate gonadotropin release from pituitary gonadotropes, the gonadotrope-derived LbetaT2 cell line was used as a model system and radioimmunoassays were employed to investigate how 5-HT3AR activation influences luteinizing hormone (LH) release. Our studies demonstrate that gonadotropin releasing hormone (GnRH)-stimulated LH release was decreased by the 5-HT3AR-specific antagonist MDL 72222 in a concentration-dependent manner. In addition, it was found that overexpressing the 5-HT3AR in LbetaT2 cells enhanced both basal and GnRH-stimulated LH release and also increased LHbeta gene promoter activity. These results suggest that the 5-HT3AR may participate in the hypothalamus-pituitary-gonadal axis at the level of the pituitary gonadotrope to mediate pituitary hormone release.
Indexed as
Identifiers
What OpenQuestion holds
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.