Research report17Beta-estradiol blocks NMDA-induced increases in regional cerebral O2 consumption

Add time:08/17/2019    Source:sciencedirect.com

We tested the hypothesis that 17beta-estradiol would reduce the cerebral O2 consumption response to stimulation of N-methyl-d-aspartate (NMDA) receptors. We determined NMDA receptor density in 10 ovariectomized Wistar female rats equally divided into a control group and 17beta-estradiol (500 μg/21 days) treated group. An autoradiographic assay using 125I-MK-801, an NMDA antagonist, was used to measure specific binding to NMDA receptors. Another 14 ovariectomized rats were separated into 17beta-estradiol and control groups to determine cerebral blood flow (14C-iodoantipyrine) and O2 consumption (microspectrophotometry). 17Beta-estradiol caused a 20% decrease in specific binding to cortical NMDA receptors. After topical cortical stimulation with 10−3M and 10−4M NMDA, blood flow increased significantly in control from 73±5 in the saline treated cortex to 110±8 ml/min/100 g with 10−3M NMDA. In contrast, there was no significant change in blood flow in the 17beta-estradiol treated animals. Cerebral O2 extraction increased significantly in the 10−3M NMDA treated cortex in both groups. Cerebral O2 consumption in the control group significantly increased by 53%, from 3.7±0.2 to 5.7±0.5 with 10−4M NMDA and 72% to 6.4±2.4 ml O2/min/100 g with 10−3M NMDA. The 17beta-estradiol group demonstrated no significant difference between the saline treated and NMDA treated cortex. Thus, 17beta-estradiol blocked the effects of NMDA on cerebral O2 consumption and this was associated with a slightly decreased number of NMDA receptors.

We also recommend Trading Suppliers and Manufacturers of 17BETA(H)-HOP-21(22)-EN-3-ONE (cas 17152-56-6). Pls Click Website Link as below: cas 17152-56-6 suppliers

Prev:Parenteral 17beta-estradiol decreases fasting blood glucose levels in non-obese mice with short-term ovariectomy
Next:Reductive 17beta-hydroxysteroid dehydrogenases which synthesize estradiol and inactivate dihydrotestosterone constitute major and concerted players in ER+ breast cancer cells)