ErbB4 point mutation in CU3 inbred rats affects gonadotropin-releasing-hormone neuronal function via compromised neuregulin-stimulated prostaglandin E2 release from astrocytes.
Animals
Astrocytes
/ drug effects
Cells, Cultured
Dinoprostone
/ metabolism
Disease Models, Animal
Disorders of Sex Development
/ drug therapy
Female
Gene Expression Regulation
/ genetics
Gonadotropin-Releasing Hormone
/ metabolism
Hypothalamus
/ cytology
Models, Molecular
Nerve Tissue Proteins
/ metabolism
Neuregulins
/ pharmacology
Neurons
/ drug effects
Point Mutation
/ genetics
Rats
Rats, Transgenic
Receptor, ErbB-4
/ genetics
Transforming Growth Factor alpha
/ metabolism
astroglia cells
epidermal growth factor
neuregulin
puberty
Journal
Glia
ISSN: 1098-1136
Titre abrégé: Glia
Pays: United States
ID NLM: 8806785
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
22
06
2018
revised:
26
08
2018
accepted:
14
09
2018
pubmed:
30
11
2018
medline:
14
5
2019
entrez:
29
11
2018
Statut:
ppublish
Résumé
Gonadotropin releasing hormone (GnRH)-secretion is not only regulated by neuronal factors but also by astroglia cells via growth factors and ErbB receptors of the epidermal growth factor family. Studies in transgenic mice carrying mutations in the ErbB receptor system experience impaired reproductive capacity. In addition, some of these animals show a typical skin phenotype with wavy hair and curly whiskers. The rat strain SPRD-CU3 (CU3), examined in this study, displays a similar skin phenotype and a significant impairment of the timing of puberty onset and reproductive performance, suggesting a disruption in the astrocytic to GnRH neuronal communication. To address this issue, we analyzed astrocytic prostaglandin E
Substances chimiques
Nerve Tissue Proteins
0
Neuregulins
0
Transforming Growth Factor alpha
0
Gonadotropin-Releasing Hormone
33515-09-2
Erbb4 protein, rat
EC 2.7.10.1
Receptor, ErbB-4
EC 2.7.10.1
Dinoprostone
K7Q1JQR04M
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
309-320Informations de copyright
© 2018 Wiley Periodicals, Inc.