Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat

Maternal dexamethasone (DEX; a glucocorticoid receptor agonist) exposure delays pubertal onset and alters reproductive behaviour in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring’s reproductive function by disrupting the gonadotropin-releasing hormo...

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Main Authors: Wei Ling Lim, Marshita Mohd Idris, Felix Suresh Kevin, Tomoko Soga, Ishwar Parhar
Format: Article
Language:English
Published: Frontiers Media S.A. 2016-08-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fendo.2016.00117/full
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spelling doaj-ac92c7d623d24b9c8e59b769f5c5b8f12020-11-24T22:44:07ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922016-08-01710.3389/fendo.2016.00117187918Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal RatWei Ling Lim0Marshita Mohd Idris1Felix Suresh Kevin2Tomoko Soga3Ishwar Parhar4Monash University MalaysiaMonash University MalaysiaMonash University MalaysiaMonash University MalaysiaMonash University MalaysiaMaternal dexamethasone (DEX; a glucocorticoid receptor agonist) exposure delays pubertal onset and alters reproductive behaviour in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring’s reproductive function by disrupting the gonadotropin-releasing hormone (GnRH) neuronal function in the brain. Therefore, this study determined the exposure of maternal DEX on the GnRH neuronal spine development and synaptic cluster inputs to GnRH neurons using transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of GnRH promoter. Pregnant females were administered with DEX (0.1mg/kg) or vehicle (VEH, water) daily during gestation day 13-20. Confocal imaging was used to examine the spine density of EGFP-GnRH neurons by three-dimensional rendering and synaptic cluster inputs to EGFP-GnRH neurons by synapsin I immunohistochemistry on postnatal day 0 (P0) males. The spine morphology and number on GnRH neurons did not change between the P0 males following maternal DEX and VEH treatment. The number of synaptic clusters within the organum vasculosum of the lamina terminalis (OVLT) was decreased by maternal DEX exposure in P0 males. Furthermore, the number and levels of synaptic cluster inputs in close apposition with GnRH neurons was decreased following maternal DEX exposure in the OVLT region of P0 males. In addition, the post synaptic marker molecule, post-synaptic density 95 was observed in GnRH neurons following both DEX and VEH treatment. These results suggest that maternal DEX exposure alters neural afferent inputs to GnRH neurons during early postnatal stage, which could lead to reproductive dysfunction during adulthood.http://journal.frontiersin.org/Journal/10.3389/fendo.2016.00117/fullPreoptic AreaReproductionglucocorticoidGnRH neuronSynapsin-I
collection DOAJ
language English
format Article
sources DOAJ
author Wei Ling Lim
Marshita Mohd Idris
Felix Suresh Kevin
Tomoko Soga
Ishwar Parhar
spellingShingle Wei Ling Lim
Marshita Mohd Idris
Felix Suresh Kevin
Tomoko Soga
Ishwar Parhar
Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
Frontiers in Endocrinology
Preoptic Area
Reproduction
glucocorticoid
GnRH neuron
Synapsin-I
author_facet Wei Ling Lim
Marshita Mohd Idris
Felix Suresh Kevin
Tomoko Soga
Ishwar Parhar
author_sort Wei Ling Lim
title Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
title_short Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
title_full Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
title_fullStr Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
title_full_unstemmed Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
title_sort maternal dexamethasone exposure alters synaptic inputs to gonadotropin-releasing hormone neurons in the early postnatal rat
publisher Frontiers Media S.A.
series Frontiers in Endocrinology
issn 1664-2392
publishDate 2016-08-01
description Maternal dexamethasone (DEX; a glucocorticoid receptor agonist) exposure delays pubertal onset and alters reproductive behaviour in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring’s reproductive function by disrupting the gonadotropin-releasing hormone (GnRH) neuronal function in the brain. Therefore, this study determined the exposure of maternal DEX on the GnRH neuronal spine development and synaptic cluster inputs to GnRH neurons using transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of GnRH promoter. Pregnant females were administered with DEX (0.1mg/kg) or vehicle (VEH, water) daily during gestation day 13-20. Confocal imaging was used to examine the spine density of EGFP-GnRH neurons by three-dimensional rendering and synaptic cluster inputs to EGFP-GnRH neurons by synapsin I immunohistochemistry on postnatal day 0 (P0) males. The spine morphology and number on GnRH neurons did not change between the P0 males following maternal DEX and VEH treatment. The number of synaptic clusters within the organum vasculosum of the lamina terminalis (OVLT) was decreased by maternal DEX exposure in P0 males. Furthermore, the number and levels of synaptic cluster inputs in close apposition with GnRH neurons was decreased following maternal DEX exposure in the OVLT region of P0 males. In addition, the post synaptic marker molecule, post-synaptic density 95 was observed in GnRH neurons following both DEX and VEH treatment. These results suggest that maternal DEX exposure alters neural afferent inputs to GnRH neurons during early postnatal stage, which could lead to reproductive dysfunction during adulthood.
topic Preoptic Area
Reproduction
glucocorticoid
GnRH neuron
Synapsin-I
url http://journal.frontiersin.org/Journal/10.3389/fendo.2016.00117/full
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