Developing Brain Glucose Transporters, Serotonin, Serotonin Transporter, and Oxytocin Receptor Expression in Response to Early-Life Hypocaloric and Hypercaloric Dietary, and Air Pollutant Exposures.
Environmental exposure
Fetal brain
Intrauterine growth restriction
Neurodevelopment
Neurotransmitters
Journal
Developmental neuroscience
ISSN: 1421-9859
Titre abrégé: Dev Neurosci
Pays: Switzerland
ID NLM: 7809375
Informations de publication
Date de publication:
2021
2021
Historique:
received:
19
07
2020
accepted:
20
01
2021
pubmed:
29
3
2021
medline:
14
1
2022
entrez:
28
3
2021
Statut:
ppublish
Résumé
Perturbed maternal diet and prenatal exposure to air pollution (AP) affect the fetal brain, predisposing to postnatal neurobehavioral disorders. Glucose transporters (GLUTs) are key in fueling neurotransmission; deficiency of the neuronal isoform GLUT3 culminates in autism spectrum disorders. Along with the different neurotransmitters, serotonin (5-HT) and oxytocin (OXT) are critical for the development of neural connectivity. Serotonin transporter (SERT) modulates synaptic 5-HT levels, while the OXT receptor (OXTR) mediates OXT action. We hypothesized that perturbed brain GLUT1/GLUT3 regulated 5-HT-SERT imbalance, which serves as a contributing factor to postnatal neuropsychiatric phenotypes, with OXT/OXTR providing a counterbalance. Employing maternal diet restriction (intrauterine growth restriction [IUGR]), high-fat (HF) dietary modifications, and prenatal exposure to simulated AP, fetal (E19) murine brain 5-HT was assessed by ELISA with SERT and OXTR being localized by immunohistochemistry and measured by quantitative Western blot analysis. IUGR with lower head weights led to a 48% reduction in male and female fetal brain GLUT3 with no change in GLUT1, when compared to age- and sex-matched controls, with no significant change in OXTR. In addition, a ∼50% (p = 0.005) decrease in 5-HT and SERT concentrations was displayed in fetal IUGR brains. In contrast, despite emergence of microcephaly, exposure to a maternal HF diet or AP caused no significant changes. We conclude that in the IUGR during fetal brain development, reduced GLUT3 is associated with an imbalanced 5-HT-SERT axis. We speculate that these early changes may set the stage for altering the 5HT-SERT neural axis with postnatal emergence of associated neurodevelopmental disorders.
Identifiants
pubmed: 33774619
pii: 000514709
doi: 10.1159/000514709
pmc: PMC8344089
mid: NIHMS1676670
doi:
Substances chimiques
Air Pollutants
0
Glucose Transport Proteins, Facilitative
0
Glucose Transporter Type 1
0
Glucose Transporter Type 3
0
OXTR protein, mouse
0
Receptors, Oxytocin
0
Serotonin Plasma Membrane Transport Proteins
0
Slc2a1 protein, mouse
0
Slc2a3 protein, mouse
0
Slc6a4 protein, mouse
0
Serotonin
333DO1RDJY
Oxytocin
50-56-6
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
27-42Subventions
Organisme : NICHD NIH HHS
ID : R01 HD041230
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD081206
Pays : United States
Informations de copyright
© 2021 The Author(s) Published by S. Karger AG, Basel.
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