Prenatal betamethasone does not affect glutamatergic or GABAergic neurogenesis in preterm newborns

L. R. Vose, G. Vinukonda, D. Diamond, R. Korumilli, F. Hu, M. T K Zia, R. Hevner, Praveen Ballabh

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Prenatal glucocorticoids (GCs) are routinely used for pregnant women in preterm labor to prevent respiratory distress syndrome and intraventricular hemorrhage in premature infants. However, the effect of antenatal GCs on neurogenesis in preterm neonates remains elusive. Herein, we hypothesized that prenatal GCs might suppress both glutamatergic and GABAergic neurogenesis in preterm rabbits and that this treatment would induce distinct changes in the expression of transcription factors regulating these developmental events. To test our hypotheses, we treated pregnant rabbits with betamethasone at E27 and E28, delivered the pups at E29 (term=32d), and assessed neurogenesis at birth and postnatal day 3. We quantified radial glia (Sox2+) and intermediate progenitor cells (Tbr2+) in the dorsal cortical subventricular zone to assess glutamatergic neuronal progenitors, and counted Nkx2.1+ and Dlx2+ cells in the ganglionic eminence to evaluate GABAergic neurogenesis. In addition, we assayed transcription factors regulating neurogenesis. We found that prenatal GCs did not affect the densities of radial glia and intermediate progenitors of glutamatergic or GABAergic neurons. The number of GABA+ interneurons in the ganglionic eminence was similar between the prenatal GC-treated pups compared to untreated controls. Moreover, the mRNA expression of transcription factors, including Pax6, Ngn1/2, Emx1/2, Insm1, Dlx1, Nkx2.1, and Gsh2, were comparable between the two groups. However, there was a transient elevation in Mash1 protein in betamethasone-treated pups relative to controls at birth. These data suggest that prenatal GC treatment does not significantly impact the balance of glutamatergic and GABAergic neurogenesis in premature infants.

Original languageEnglish (US)
Pages (from-to)148-157
Number of pages10
JournalNeuroscience
Volume270
DOIs
StatePublished - Jun 13 2014
Externally publishedYes

Fingerprint

Betamethasone
Neurogenesis
Glucocorticoids
Newborn Infant
Transcription Factors
Premature Infants
Neuroglia
Rabbits
GABAergic Neurons
Premature Obstetric Labor
Lateral Ventricles
Interneurons
Contraception
gamma-Aminobutyric Acid
Pregnant Women
Stem Cells
Parturition
Hemorrhage
Messenger RNA
Therapeutics

Keywords

  • Betamethasone
  • GABAergic
  • Glucocorticoid
  • Glutamatergic
  • Neurogenesis
  • Prematurity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Medicine(all)

Cite this

Prenatal betamethasone does not affect glutamatergic or GABAergic neurogenesis in preterm newborns. / Vose, L. R.; Vinukonda, G.; Diamond, D.; Korumilli, R.; Hu, F.; Zia, M. T K; Hevner, R.; Ballabh, Praveen.

In: Neuroscience, Vol. 270, 13.06.2014, p. 148-157.

Research output: Contribution to journalArticle

Vose, L. R. ; Vinukonda, G. ; Diamond, D. ; Korumilli, R. ; Hu, F. ; Zia, M. T K ; Hevner, R. ; Ballabh, Praveen. / Prenatal betamethasone does not affect glutamatergic or GABAergic neurogenesis in preterm newborns. In: Neuroscience. 2014 ; Vol. 270. pp. 148-157.
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AU - Vinukonda, G.

AU - Diamond, D.

AU - Korumilli, R.

AU - Hu, F.

AU - Zia, M. T K

AU - Hevner, R.

AU - Ballabh, Praveen

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