Stroke-induced changes in estrogen release and ...



Title Stroke-induced changes in estrogen release and neuronal activity in the parabrachial nucleus of the male rat
Author(s) T. M. Saleh, B. J. Connell, C. Legge, A. E. Cribb
Journal Journal of Stroke and Cerebrovascular Diseases : The Official Journal of National Stroke Association
Date 2004
Volume 13
Issue 1
Start page 24
End page 34
Abstract Recent investigations have provided evidence to suggest exogenous estrogen administration into autonomic nuclei prevents or reverses the autonomic dysfunction observed after middle cerebral artery occlusion (MCAO) in male rats. Because estrogen seems to be a potent neuroprotectant against autonomic dysfunction, it is our hypothesis that endogenous estrogen levels within autonomic nuclei will increase in response to stroke. Therefore, in this investigation, in vivo microdialysis was used to simultaneously measure the concentration of estrogen in the plasma and in the parabrachial nucleus (PBN) of male Sprague-Dawley rats after MCAO. Analysis of dialysate samples before MCAO and in sham-operated controls revealed a baseline concentration of estrogen in the PBN (38 +/- 3 pg/mL; n = 36), which was significantly greater than that found in plasma (22 +/- 6 pg/mL; n = 6; P < .05). The concentration of estrogen in the PBN was significantly increased immediately after MCAO (85 +/- 4 pg/mL; n = 7; P < .05) but then decreased to below pre-MCAO values (12 +/- 2 pg/mL; n = 7; P < .05) by 90 minutes after MCAO and remained below baseline levels until the end of the experiment (240 minutes post-MCAO). No changes in plasma estrogen levels were detected at any time point after MCAO. In addition, extracellular electrophysiological recordings from PBN neurons revealed that MCAO resulted in an immediate decrease in the activity of PBN neurons, which was completely blocked after systemic estrogen injection. These results suggest that estrogen is released into the PBN in response to MCAO and that the source of estrogen seems to be primarily caused by terminal release as opposed to increased local synthesis.
DOI 10.1016/j.jstrokecerebrovasdis.2004.01.003

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