Neuroreport. 2014 Jan 22;25(2):100-4. doi: 10.1097/WNR.0000000000000052.

Estradiol decreases rat depressive behavior by estrogen receptor beta but

not alpha: no correlation with plasma corticosterone.
Yang F1, Tao J, Xu L, Zhao N, Chen J, Chen W, Zhu Y, Qiu J.
Author information
Abstract
17-Estradiol (E2) may influence some of the sex differences in stress-related
neuropsychiatric disorders, such as anxiety and depression. E2 may also modulate
the hypothalamic-pituitary-adrenal axis function as a cortisol response to stress in
women. This study explored the role of E2 (10 and 50 g/rat) and
selective estrogen receptor modulators: diarylpropionitrile (DPN, 10 g/rat) and
propyl pyrazole triol (PPT, 10 g/rat), in anxiety anddepressive behaviors in
ovariectomized rats using an animal model. The study also examined the
relationship between rats' affective behavior and the plasma corticosterone (CORT)
levels in response to chronic repeated restraint stress and series of behavior tests.
Ovariectomized rats administered 10 g E2 and 10 g DPN showed
more central entries in the open field, more open-arm duration in the elevated plus
maze, and less immobility duration in the forced-swim test compared with rats
administered vehicle or 10 g PPT. 10 and 50 g E2 significantly increased plasma
CORT levels when compared with vehicle, 10 g DPN, or 10 g PPT. There was no
correlation between the rats' depressive behavior and their plasma CORT levels.
These results suggest that the antidepressant effects of E2 may involve ER, but
are independent of an enhanced CORT response to stress.

Effect of estradiol on MAPK p44/42 expression in the brain induced by

angiotensin II (LB709)
1. Gislaine Almeida-Pereira1, Ricardo Coletti1, Andr Mecawi1, Lucila
Elias1 and
2. Jos Antunes-Rodrigues1
+Author Affiliations
1.

Physiology University of Sao Paulo, School of Medicine of Ribeirao Preto

Ribeirao Preto Brazil

Abstract
This study aims to investigate the influence of estradiol on the MAPK p44/42
expression in the lamina terminalis and hypothalamic nucleus induced by central

stimulation angiotensinergic. Wistar rats (~250g) were submitted to ovariectomy

and on the following day they were treated with estradiol cypionate (10g/rat, sc) or
vehicle (corn oil, 0.1mL/rat, sc) for eight days. On the eighth day, these rats were
submitted to icv (lateral ventricle) administration of angiotensin II (ANGII,
25ng/2L/rat) or vehicle (0.9% saline, 2L/rat). Ten min after the animals were
decapitated for brain collection and MAPK p44/42 analysis by western blotting. Data
were analyzed using Student t test and the level of significance was set at 5%. The
pretreatment with estradiol attenuated the MAPK p44/42 total expression in the
lamina terminalis and paraventricular and supraoptic nucleus (t(12)=3.8; t(10)=3.5,
respectively) in comparison with rats treatment oil and saline icv. Both ANG II and
estradiol increased the phosphorylation of the MAPK p44/42 in lamina terminalis and
hypothalamic nucleus in comparison with rats treatment oil and saline icv (t(12)=3.75, t(13)=-2.81, t(14)=-3.85, t(14)=-4.15, respectively). However ANG II did not
further increase the phosphorylation of MAPK p44/42 induced by estradiol in all
structures analyzes. These result suggest that the known effect of estradiol on the
responses behaviors and neuroendocrine induced by ANG II can be due to change of
MAPK p44/42 phosphorylation this structures central involved with control body
fluids.