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. 2021;19(3):383-391.
doi: 10.2174/1570159X18666200429232104.

Antiepileptogenic Effect of Retinoic Acid

Artemio Rosiles-Abonce  1 , Carmen Rubio  2 , Elisa Taddei  1 , Dulce Rosiles  1 , Moisés Rubio-Osornio  1
Affiliations

Antiepileptogenic Effect of Retinoic Acid

Artemio Rosiles-Abonce et al. Curr Neuropharmacol. 2021.

Abstract

Retinoic acid, a metabolite of vitamin A, acts through either genomic or nongenomic actions. The genomic action of retinoids exerts effects on gene transcription through interaction with retinoid receptors such as retinoic acid receptors (RARα, β, and γ) and retinoid X receptors (RXRα, β, and γ) that are primarily concentrated in the amygdala, pre-frontal cortex, and hippocampal areas in the brain. In response to retinoid binding, RAR/RXR heterodimers undergo major conformational changes and orchestrate the transcription of specific gene networks. Previous experimental studies have reported that retinoic acid exerts an antiepileptogenic effect through diverse mechanisms, including the modulation of gap junctions, neurotransmitters, long-term potentiation, calcium channels and some genes. To our knowledge, there are no previous or current clinical trials evaluating the use of retinoic acid for seizure control.

Keywords: Epilepsy; antiepileptic; genes; retinoic acid; retinoids; seizures.

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Figures

Fig. (1)
Fig. (1)
Signaling of retinoids. Retinyl esters, retinol, and β-carotene are taken into the body from the diet. Both retinol and β-carotene may be converted into the transcriptionally active vitamin A forms after first being converted to retinaldehyde. Retinoic acid then regulates transcription of vitamin A responsive genes. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
Fig. (2)
Fig. (2)
Main mechanisms of retinol in seizures (1) Gap junctions: retinoic acid is a gap junction blocker. (2) Inhibitory synaptic transmission: significant reduction of inhibitory synaptic transmission. (3) Long-term potentiation: retinoic acid treatment blocks expression of long-term potentiation. (4) Voltage-gated calcium channels: retinoic acid inhibits neuronal voltage-gated calcium channels. (5) Electroencephalography findings: decreased delta and increased theta activity. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
See this image and copyright information in PMC

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