Preprint Short Note Version 1 Preserved in Portico This version is not peer-reviewed

Synaptic Plasticity is Altered by Supraphysiological 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)

How to cite: Duester, G. Synaptic Plasticity is Altered by Supraphysiological Levels of Retinoic Acid Acting Nongenomically however Endogenous Retinoic Acid Has Not Been Shown to Control Synaptic Plasticity. Preprints 2021, 2021110412 (doi: 10.20944/preprints202111.0412.v1). Duester, G. Synaptic Plasticity is Altered by Supraphysiological Levels of Retinoic Acid Acting Nongenomically however Endogenous Retinoic Acid Has Not Been Shown to Control Synaptic Plasticity. Preprints 2021, 2021110412 (doi: 10.20944/preprints202111.0412.v1).

Abstract

A paper recently published on forebrain cortical synaptic plasticity reports that retinoic acid (RA) induces synaptopodin-dependent metaplasticity in mouse dentate granule cells (Lenz et al., 2021). Retinoic acid (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, Lenz et al. report that RA functions in a nongenomic fashion to control forebrain cortical synaptic plasticity which modulates synaptic transmission to effectively respond to specific stimuli; specifically, they report that this nongenomic response occurs in the dorsal hippocampus but not ventral hippocampus. They performed RA treatment studies which provided information on how a supraphysiological level of RA effects synaptic plasticity. However, the authors did not perform an RA loss-of-function study to verify that endogenous RA is required for synaptic plasticity.

Keywords

synaptic plasticity; retinoic acid; nongenomic action

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