ArticlePsychopharmacology2015
Role of nitric oxide in the behavioral and neurochemical effects of IB-MECA in zebrafish.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Anxiolytic-like effects of acute serotonin-releasing agents in zebrafish models of anxiety: experimental study and systematic review.Acta neuropsychiatrica · 2024Pooled it
- Nitrergic Signaling Mediation of Neurobehavioral Responses to Stress in Zebrafish.Journal of neurochemistry · 2025Review
- Article
- Non-mammalian models in behavioral neuroscience: consequences for biological psychiatry.Frontiers in behavioral neuroscience · 2015Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe adenosine A3 receptor and the nitric oxide (NO) pathway regulate the function and localization of serotonin transporters (SERTs). These transporters regulate extracellular serotonin levels, which are correlated with defensive behavior.
objectiveThe purpose of this study was to understand the role of the A3AR on anxiety and arousal models in zebrafish, and whether this role is mediated by the nitrergic modulation of serotonin uptake.
methodsThe effects of IB-MECA (0.01 and 0.1 mg/kg) were assessed in a series of behavioral tasks in adult zebrafish, as well as on extracellular serotonin levels in vivo and serotonin uptake in brain homogenates. Finally, the interaction between IB-MECA and drugs blocking voltage-dependent calcium channels (VDCCs), NO synthase, and SERT was analyzed.
resultsAt the lowest dose, IB-MECA decreased bottom dwelling and scototaxis, while at the highest dose, it also decreased shoaling, startle probability, and melanophore responses. These effects were accompanied by an increase in brain extracellular serotonin levels. IB-MECA also concentration-dependently increased serotonin uptake in vitro. The effects of IB-MECA on extracellular 5-HT, scototaxis, and geotaxis were blocked by L-NAME, while only the effects on 5-HT and scototaxis were blocked by verapamil. In vitro, the increase in 5-HT uptake was dependent on VDCCs and NO. Finally, fluoxetine blocked the effect of IB-MECA on scototaxis, but not geotaxis.
conclusionThese results suggest that the effect of IB-MECA on scototaxis are mediated by a VDCC-NO-SERT pathway. While NO seems to mediate the effects of IB-MECA on geotaxis, neither VDCCs nor SERT seems to be involved in this process.
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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 Socratic graph.