ReviewFrontiers in neuroendocrinology2023
Insufficient support for retinoic acid receptor control of synaptic plasticity through a non-genomic mechanism.
Review in Frontiers in neuroendocrinology, 2023. 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, 2 citations in OpenAlex.
- Early retinoic acid signaling organizes the body axis and defines domains for the forelimb and eye.Current topics in developmental biology · 2025Review
- Non-canonical retinoid signaling in neural development, regeneration and synaptic function.Frontiers in molecular neuroscience · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
It is well established that retinoic acid receptors (RARs) function as nuclear receptors that control gene expression in response to binding of the ligand retinoic acid (RA). However, some studies have proposed that RAR-alpha (RARa) controls synaptic plasticity via non-genomic effects outside the nucleus, i.e. effects on mRNA translation of GluA1, a sub-unit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor. In order to support this non-genomic mechanism, studies have reported RARa knockout mice or treatment with pharmacological levels of RA and RAR antagonists to propose that RARa is required to control normal synaptic plasticity. A major shortcoming of the non-genomic hypothesis is that there have been no mutational studies showing that RARa can bind the GluA1 mRNA to control GLUA1 protein levels in a non-genomic manner. Also, without a genetic study that removes the endogenous ligand RA, it is impossible to conclude that RARa and its ligand RA control synaptic plasticity through a non-genomic signaling mechanism.
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.