Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats

Prenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is unknown whether the 5-hydroxytryptamine 2A receptor (5-HT 2A R) is involved in the effects of prenatal alcohol exp...

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Main Authors: Ming-li Ji, Yun-hong Wu, Zhi-bin Qian
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2015-01-01
Series:Neural Regeneration Research
Subjects:
Online Access:http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=7;spage=1095;epage=1100;aulast=Ji
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spelling doaj-c90b55fa5f64480290ac103e50f9f74a2020-11-25T02:00:31ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742015-01-011071095110010.4103/1673-5374.160101Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal ratsMing-li JiYun-hong WuZhi-bin QianPrenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is unknown whether the 5-hydroxytryptamine 2A receptor (5-HT 2A R) is involved in the effects of prenatal alcohol exposure. In the present study, pregnant female rats received drinking water containing alcohol at concentrations of 0%, 1%, 2%, 4%, 8% or 10% (v/v) throughout the gestation period. Slices of the medulla from 2-day-old neonatal rats were obtained to record respiratory rhythmical discharge activity. 5-HT 2A R protein and mRNA levels in the pre-Bötzinger complex of the respiratory center were measured by western blot analysis and quantitative RT-PCR, respectively. Compared with the 0% alcohol group, respiratory rhythmical discharge activity in medullary slices in the 4%, 8% and 10% alcohol groups was decreased, and the reduction was greatest in the 8% alcohol group. Respiratory rhythmical discharge activity in the 10% alcohol group was irregular. Thus, 8% was the most effective alcohol concentration at attenuating respiratory rhythmical discharge activity. These findings suggest that prenatal alcohol exposure attenuates respiratory rhythmical discharge activity in neonatal rats by downregulating 5-HT 2A R protein and mRNA levels.http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=7;spage=1095;epage=1100;aulast=Jinerve regeneration; brain injury; prenatal alcohol exposure; pre-Bötzinger complex; respiratory depression; neonatal rats; medullary slice; medullary respiratory center; respiratory rhythmical discharge activity; respiratory neuron; 5-hydroxytryptamine 2A receptor; neural regeneration
collection DOAJ
language English
format Article
sources DOAJ
author Ming-li Ji
Yun-hong Wu
Zhi-bin Qian
spellingShingle Ming-li Ji
Yun-hong Wu
Zhi-bin Qian
Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
Neural Regeneration Research
nerve regeneration; brain injury; prenatal alcohol exposure; pre-Bötzinger complex; respiratory depression; neonatal rats; medullary slice; medullary respiratory center; respiratory rhythmical discharge activity; respiratory neuron; 5-hydroxytryptamine 2A receptor; neural regeneration
author_facet Ming-li Ji
Yun-hong Wu
Zhi-bin Qian
author_sort Ming-li Ji
title Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
title_short Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
title_full Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
title_fullStr Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
title_full_unstemmed Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats
title_sort neurotoxicity of prenatal alcohol exposure on medullary pre-bötzinger complex neurons in neonatal rats
publisher Wolters Kluwer Medknow Publications
series Neural Regeneration Research
issn 1673-5374
publishDate 2015-01-01
description Prenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is unknown whether the 5-hydroxytryptamine 2A receptor (5-HT 2A R) is involved in the effects of prenatal alcohol exposure. In the present study, pregnant female rats received drinking water containing alcohol at concentrations of 0%, 1%, 2%, 4%, 8% or 10% (v/v) throughout the gestation period. Slices of the medulla from 2-day-old neonatal rats were obtained to record respiratory rhythmical discharge activity. 5-HT 2A R protein and mRNA levels in the pre-Bötzinger complex of the respiratory center were measured by western blot analysis and quantitative RT-PCR, respectively. Compared with the 0% alcohol group, respiratory rhythmical discharge activity in medullary slices in the 4%, 8% and 10% alcohol groups was decreased, and the reduction was greatest in the 8% alcohol group. Respiratory rhythmical discharge activity in the 10% alcohol group was irregular. Thus, 8% was the most effective alcohol concentration at attenuating respiratory rhythmical discharge activity. These findings suggest that prenatal alcohol exposure attenuates respiratory rhythmical discharge activity in neonatal rats by downregulating 5-HT 2A R protein and mRNA levels.
topic nerve regeneration; brain injury; prenatal alcohol exposure; pre-Bötzinger complex; respiratory depression; neonatal rats; medullary slice; medullary respiratory center; respiratory rhythmical discharge activity; respiratory neuron; 5-hydroxytryptamine 2A receptor; neural regeneration
url http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=7;spage=1095;epage=1100;aulast=Ji
work_keys_str_mv AT mingliji neurotoxicityofprenatalalcoholexposureonmedullaryprebotzingercomplexneuronsinneonatalrats
AT yunhongwu neurotoxicityofprenatalalcoholexposureonmedullaryprebotzingercomplexneuronsinneonatalrats
AT zhibinqian neurotoxicityofprenatalalcoholexposureonmedullaryprebotzingercomplexneuronsinneonatalrats
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