Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.

Thyroid hormones are messengers that bind to specific nuclear receptors and regulate a wide range of physiological processes in the early stages of vertebrate embryonic development, including neurodevelopment and myelogenesis. We here tested the effects of reduced T3 availability upon the myelinatio...

Full description

Bibliographic Details
Main Authors: Brenda Minerva Farías-Serratos, Iván Lazcano, Patricia Villalobos, Veerle M Darras, Aurea Orozco
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2021-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0256207
_version_ 1819093856985022464
author Brenda Minerva Farías-Serratos
Iván Lazcano
Patricia Villalobos
Veerle M Darras
Aurea Orozco
author_facet Brenda Minerva Farías-Serratos
Iván Lazcano
Patricia Villalobos
Veerle M Darras
Aurea Orozco
author_sort Brenda Minerva Farías-Serratos
collection DOAJ
description Thyroid hormones are messengers that bind to specific nuclear receptors and regulate a wide range of physiological processes in the early stages of vertebrate embryonic development, including neurodevelopment and myelogenesis. We here tested the effects of reduced T3 availability upon the myelination process by treating zebrafish embryos with low concentrations of iopanoic acid (IOP) to block T4 to T3 conversion. Black Gold II staining showed that T3 deficiency reduced the myelin density in the forebrain, midbrain, hindbrain and the spinal cord at 3 and 7 dpf. These observations were confirmed in 3 dpf mbp:egfp transgenic zebrafish, showing that the administration of IOP reduced the fluorescent signal in the brain. T3 rescue treatment restored brain myelination and reversed the changes in myelin-related gene expression induced by IOP exposure. NG2 immunostaining revealed that T3 deficiency reduced the amount of oligodendrocyte precursor cells in 3 dpf IOP-treated larvae. Altogether, the present results show that inhibition of T4 to T3 conversion results in hypomyelination, suggesting that THs are part of the key signaling molecules that control the timing of oligodendrocyte differentiation and myelin synthesis from very early stages of brain development.
first_indexed 2024-12-21T23:18:10Z
format Article
id doaj.art-49f6facb2dc04d1cbf279d43029d468f
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-12-21T23:18:10Z
publishDate 2021-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-49f6facb2dc04d1cbf279d43029d468f2022-12-21T18:46:50ZengPublic Library of Science (PLoS)PLoS ONE1932-62032021-01-01168e025620710.1371/journal.pone.0256207Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.Brenda Minerva Farías-SerratosIván LazcanoPatricia VillalobosVeerle M DarrasAurea OrozcoThyroid hormones are messengers that bind to specific nuclear receptors and regulate a wide range of physiological processes in the early stages of vertebrate embryonic development, including neurodevelopment and myelogenesis. We here tested the effects of reduced T3 availability upon the myelination process by treating zebrafish embryos with low concentrations of iopanoic acid (IOP) to block T4 to T3 conversion. Black Gold II staining showed that T3 deficiency reduced the myelin density in the forebrain, midbrain, hindbrain and the spinal cord at 3 and 7 dpf. These observations were confirmed in 3 dpf mbp:egfp transgenic zebrafish, showing that the administration of IOP reduced the fluorescent signal in the brain. T3 rescue treatment restored brain myelination and reversed the changes in myelin-related gene expression induced by IOP exposure. NG2 immunostaining revealed that T3 deficiency reduced the amount of oligodendrocyte precursor cells in 3 dpf IOP-treated larvae. Altogether, the present results show that inhibition of T4 to T3 conversion results in hypomyelination, suggesting that THs are part of the key signaling molecules that control the timing of oligodendrocyte differentiation and myelin synthesis from very early stages of brain development.https://doi.org/10.1371/journal.pone.0256207
spellingShingle Brenda Minerva Farías-Serratos
Iván Lazcano
Patricia Villalobos
Veerle M Darras
Aurea Orozco
Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
PLoS ONE
title Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
title_full Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
title_fullStr Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
title_full_unstemmed Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
title_short Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.
title_sort thyroid hormone deficiency during zebrafish development impairs central nervous system myelination
url https://doi.org/10.1371/journal.pone.0256207
work_keys_str_mv AT brendaminervafariasserratos thyroidhormonedeficiencyduringzebrafishdevelopmentimpairscentralnervoussystemmyelination
AT ivanlazcano thyroidhormonedeficiencyduringzebrafishdevelopmentimpairscentralnervoussystemmyelination
AT patriciavillalobos thyroidhormonedeficiencyduringzebrafishdevelopmentimpairscentralnervoussystemmyelination
AT veerlemdarras thyroidhormonedeficiencyduringzebrafishdevelopmentimpairscentralnervoussystemmyelination
AT aureaorozco thyroidhormonedeficiencyduringzebrafishdevelopmentimpairscentralnervoussystemmyelination