The effects of ovarian hormones on stressor-induced hormonal responses, glucocorticoid receptor expression and translocation, and genes related to receptor signaling in adult female rats

Autor: Marina L. Marcolin, Cheryl M. McCormick, Matthew R. Green
Rok vydání: 2017
Předmět:
0301 basic medicine
Restraint
Physical

medicine.medical_specialty
Physiology
Ovariectomy
Hippocampal formation
Hippocampus
Tacrolimus Binding Proteins
03 medical and health sciences
Behavioral Neuroscience
chemistry.chemical_compound
0302 clinical medicine
Glucocorticoid receptor
Receptors
Glucocorticoid

Corticosterone
Stress
Physiological

Internal medicine
medicine
Hippocampus (mythology)
Animals
Rats
Long-Evans

Receptor
Progesterone
Estradiol
Endocrine and Autonomic Systems
business.industry
Rats
DNA-Binding Proteins
Psychiatry and Mental health
030104 developmental biology
Neuropsychology and Physiological Psychology
Glucocorticoid secretion
Endocrinology
chemistry
Ovariectomized rat
Female
business
hormones
hormone substitutes
and hormone antagonists

030217 neurology & neurosurgery
Stress
Psychological

Hormone
Signal Transduction
Transcription Factors
Zdroj: Stress (Amsterdam, Netherlands). 21(2)
ISSN: 1607-8888
Popis: Estradiol potentiates hypothalamic-pituitary-adrenal activity and delays the return of glucocorticoid secretion to baseline after a stressor exposure in female rats; we investigated whether estradiol effects involve actions on glucocorticoid receptor (GR) translocation and expression of receptor co-chaperones. In Experiment 1 intact females and ovariectomized (OVX) females were treated for four days with vehicle (VEH), 17β-estradiol benzoate (EB), or EB and progesterone (EB + P). Samples were taken from rats in the home cage (baseline) or after 30 min of restraint stress in a plastic restrainer (post-restraint) (n = 10/group). OVX-VEH treatment reduced baseline and post-restraint plasma concentrations of corticosterone versus all other treatments. Western blots indicated that OVX-VEH treated rats had greater hippocampal cytosolic GR expression than other treatments. Stress increased hippocampal nuclear GR expression, but without treatment differences. In Experiment 2 OVX rats were treated daily with VEH, EB, or EB + P (n = 8/group). OVX-VEH rats showed a lower stimulation of corticosterone secretion by restraint stress than other treatments and OVX-EB + P treated rats had lower concentrations than the OVX-EB group, suggesting progesterone mitigated estradiol effects. Quantitative polymerase chain reaction experiments indicated that stress increased Fkbp5 mRNA in the ventral hippocampus, with no effect of stress or treatment on Nr3c1 (GR), Nr3c2 (MR), Fkbp4, Bag1, or Ncoa1 (SRC-1) expression. Thus, the hypothesis is that estradiol effects on negative feedback are mediated by altered expression of receptor co-chaperones or co-modulators in the hippocampus was not supported. Estradiol may blunt feedback by limiting the availability of cytosolic GR protein.
Databáze: OpenAIRE