ArticleJournal of neurophysiology2010
Nitric oxide potentiates cAMP-gated cation current by intracellular acidification in feeding neurons of pleurobranchaea.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Intraoperative management during liver transplantation in the child with mitochondrial depletion syndrome: A case report.International journal of surgery case reports · 2024Article
- Combinatorial roles of mitochondria and cGMP/PKG pathway in the generation of neuronal free Zn2+ under the presence of nitric oxide.Journal of the Chinese Medical Association : JCMA · 2020Article
- A review of the actions of Nitric Oxide in development and neuronal function in major invertebrate model systems.AIMS neuroscience · 2019Review
- cAMP, CaACS chemical neuroscience · 2018Review
- Small-volume analysis of cell-cell signaling molecules in the brain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Review
- Effect of nitric oxide donors S-nitroso-N-acetyl-DL-penicillamine, spermine NONOate and propylamine propylamine NONOate on intracellular pH in cardiomyocytes.Clinical and experimental pharmacology & physiology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
A pH-sensitive cAMP-gated cation current (I(Na,cAMP)) is widely distributed in neurons of the feeding motor networks of gastropods. In the sea slug Pleurobranchaea this current is potentiated by nitric oxide (NO), which itself is produced by many feeding neurons. The action of NO is not dependent on either cGMP or cAMP signaling pathways. However, we found that NO potentiation of I(Na,cAMP) in the serotonergic metacerebral cells could be blocked by intracellular injection of MOPS buffer (pH 7.2). In neurons injected with the pH indicator BCECF, NO induced rapid intracellular acidification to several tenths of a pH unit. Intracellular pH has not previously been identified as a specific target of NO, but in this system NO modulation of I(Na,cAMP) via pH(i) may be an important regulator of the excitability of the feeding motor network.
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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.