PreprintShort NoteVersion 2Preserved in Portico This version is not peer-reviewed
Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity
Version 1
: Received: 20 November 2021 / Approved: 23 November 2021 / Online: 23 November 2021 (08:39:11 CET)
Version 2
: Received: 8 December 2021 / Approved: 9 December 2021 / Online: 9 December 2021 (15:08:49 CET)
How to cite:
Duester, G. Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity. Preprints2021, 2021110412. https://doi.org/10.20944/preprints202111.0412.v2
Duester, G. Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity. Preprints 2021, 2021110412. https://doi.org/10.20944/preprints202111.0412.v2
Duester, G. Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity. Preprints2021, 2021110412. https://doi.org/10.20944/preprints202111.0412.v2
APA Style
Duester, G. (2021). Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity. Preprints. https://doi.org/10.20944/preprints202111.0412.v2
Chicago/Turabian Style
Duester, G. 2021 "Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticity" Preprints. https://doi.org/10.20944/preprints202111.0412.v2
Abstract
A paper recently published by eLife on forebrain cortical synaptic plasticity reports that retinoic acid (RA) alters synaptopodin-dependent metaplasticity in mouse dentate granule cells (Lenz et al., 2021). RA is the active form of vitamin A that functions as a ligand for nuclear RA receptors that directly bind genomic control regions to regulate gene expression (Chambon, 1996; Ghyselinck and Duester, 2019). However, some studies have suggested that RA may have nongenomic effects outside of the nucleus, particularly with regard to synaptic plasticity (Aoto et al., 2008; Zhang et al., 2018). The current results reported by Lenz et al. demonstrate that treatment with pharmacological levels of RA can alter synaptic plasticity which may be useful to treat neurological diseases (Lenz et al., 2021). However, the results reported here and those reported by others have not shown that endogenous RA is normally required for synaptic plasticity (or any other nongenomic effect) as there are no reports of genetic loss-of-function studies that remove endogenous RA in adult brain. The implication is that pharmacological levels of RA result in nongenomic effects, some of which may be helpful to treat certain diseases but in other cases this may cause unwanted side-effects.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received:
9 December 2021
Commenter:
Gregg Duester
Commenter's Conflict of Interests:
Author
Comment:
The Article was Changed a Little. Plus, the Article Now More Accurately Describes the Difference between Pharmacological and Endogenous Retinoic Acid Action
Commenter: Gregg Duester
Commenter's Conflict of Interests: Author