ArticleNeurochemical research2002
Pertussis toxin-sensitive G proteins mediate the inhibition of basal phosphoinositide metabolism caused by adenosine A1 receptors in rat hippocampal slices.
Article in Neurochemical research, 2002. 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.
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
2 citing papers in PubMed, 8 citations in OpenAlex.
- The Signaling Pathways Involved in the Anticonvulsive Effects of the Adenosine AInternational journal of molecular sciences · 2020Review
- The Role of cGMP on Adenosine A 1 Receptor-mediated Inhibition of Synaptic Transmission at the Hippocampus.Frontiers in pharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adenosine A1 receptor selective agonist, N6-cyclopentyladenosine (CPA, 300 nM) inhibited basal accumulation of [3H]inositol phosphates ([3H]InsPs), but not the total levels of membrane [3H]-phosphoinositides, in rat hippocampal slices. This action of CPA was not significantly modified when synaptic transmission was blocked with tetrodotoxin (TTX, 200 nM) but was prevented in slices pre-incubated with pertussis toxin (PTX, 5 microg/mL) for 12-16 hr. Neither PTX nor TTX, when applied in the absence of CPA, influenced basal [3H]InsPs accumulation. It is concluded that the inhibition of the basal phosphatidylinositol metabolism by adenosine A1 receptor activation is independent of neurotransmission and involves a PTX-sensitive G protein, probably of the Gi/Go family.
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Registered trials
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