ArticleNaunyn-Schmiedeberg's archives of pharmacology1995
Cultured chick sympathetic neurons: prostanoid EP1 receptor-mediated facilitation of noradrenaline release.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed, 11 citations in OpenAlex.
- Functional prostaglandin E (EP) receptors in human penile corpus cavernosum.International journal of impotence research · 2003Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostanoid EP receptor-mediated modulation of noradrenaline release from cultured chick sympathetic neurons was investigated. Transmitter release from dissociated cell cultures of embryonic paravertebral ganglia, loaded with [3H]-noradrenaline, was elicited either by electrical field stimulation (36 pulses/3 Hz) or by elevating the extracellular concentration of K+ (to 30 mM; for 2 min). Prostaglandin E2 (PGE2; 0.01-3 microM) enhanced electrically evoked [3H]-noradrenaline release in a concentration-dependent manner with a maximal increase by about 50% at 1 microM. Also iloprost (0.1-3 microM) increased transmitter release concentration- dependently, whereas misoprostol (0.1-3 microM) had no effect. Indometacin (10 microM) influenced neither evoked release per se nor the enhancement caused by PGE2- AH6809 (3 microM), a selective EP1 receptor antagonist, blocked the enhancement caused by both PGE2 and iloprost K(+)-evoked noradrenaline release, which was virtually insensitive to tetrodotoxin (0.3 microM), was increased by PGE2 to an extent comparable to that observed after electrical stimulation. In summary, the present data indicate that PGE2 facilitates noradrenaline release from cultured chick sympathetic neurons by a receptor which shows the pharmacological profile of the EP1 subtype and is probably located at the processes of the neuron.
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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.