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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

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Selective Oestrogen Receptor Agonists Rescued Hippocampus Parameters in Male Spontaneously Hypertensive Rats.

L Pietranera^1,2, J Correa¹, M E Brocca¹

¹Laboratory of Neuroendocrine Biochemistry, Instituto de Biología y Medicina Experimental, Buenos Aires, Argentina.

Journal of Neuroendocrinology

|August 13, 2016

Summary

This summary is machine-generated.

Diarylpropionitrite (DPN), an estrogen receptor beta agonist, improved brain health in hypertensive rats by reducing inflammation and boosting neurogenesis. Propylpyrazole triol (PPT), an estrogen receptor alpha agonist, had limited effects.

Keywords:

hippocampus hypertension neurogenesis oestrogen receptors

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Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration

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Published on: June 7, 2012

Area of Science:

Neuroscience
Endocrinology
Cardiovascular Research

Background:

Spontaneously hypertensive rats (SHR) exhibit hippocampal damage, including reduced brain-derived neurotrophic factor (BDNF) and neurogenesis.
These alterations are reversed by 17β-estradiol, suggesting a role for estrogen receptors (ERs).

Purpose of the Study:

To investigate the specific roles of ERα and ERβ in mediating the neuroprotective effects of estrogen in SHR.
To determine if ERα or ERβ activation influences hippocampal BDNF expression, neurogenesis, astrogliosis, and aromatase levels in SHR.

Main Methods:

Male SHR and Wistar Kyoto rats were treated for two weeks with ERα agonist (propylpyrazole triol, PPT) or ERβ agonist (diarylpropionitrite, DPN).
Immunocytochemistry was used to quantify astrocytes (GFAP+), neuronal progenitors (DCX+), and aromatase.
Brain-derived neurotrophic factor (BDNF) mRNA levels were measured using quantitative polymerase chain reaction.

Main Results:

DPN treatment decreased blood pressure, reduced astrogliosis, increased BDNF mRNA, and enhanced DCX+ progenitor numbers in SHR.
PPT treatment decreased astrogliosis and slightly increased BDNF mRNA but did not affect blood pressure or DCX+ progenitors.
Aromatase staining increased with PPT but remained unchanged with DPN treatment in SHR.

Conclusions:

Estrogen receptor beta (ERβ) activation, via DPN, appears to preferentially promote BDNF expression and neurogenesis in the hippocampus of hypertensive rats.
While both ERα and ERβ may contribute to estrogen's neuroprotection, ERβ activation shows more significant benefits for neurogenesis and blood pressure regulation in this model.
These findings suggest potential therapeutic strategies targeting ERβ for hypertension-related encephalopathy.