Estrogen in the parabrachial nucleus attenuates the sympathoexcitation following MCAO in male rats

Recent investigations have provided evidence to suggest systemic estrogen administration prevented or reversed the sympathoexcitation observed following middle cerebral artery occlusion (MCAO) in male rats. The present investigation sought to determine the role of estrogen injected directly into the...

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Veröffentlicht in:Brain research 2005-12, Vol.1066 (1), p.187-195
Hauptverfasser: Saleh, Tarek M., Connell, Barry J., Cribb, Alastair E.
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Sprache:eng
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Zusammenfassung:Recent investigations have provided evidence to suggest systemic estrogen administration prevented or reversed the sympathoexcitation observed following middle cerebral artery occlusion (MCAO) in male rats. The present investigation sought to determine the role of estrogen injected directly into the parabrachial nucleus (PBN) on the MCAO-induced sympathoexcitation as well as the role of the rostral ventrolateral medulla (RVLM) in mediating the sympathoexcitatory response. Male Sprague–Dawley rats were anesthetized with sodium thiobutabarbitol (100 mg/kg) and were instrumented to continuously record blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Following occlusion of the middle cerebral artery, there was a significant increase in RSNA (from 3.8 ± 0.4 to 8.3 ± 0.6 μV/s; P  0.05). Extracellular electrophysiological recordings from RVLM neurons demonstrated that MCAO did not produce any significant change in neuronal activity over the experimental time course ( P > 0.05). Also, bilateral injection of estrogen into the PBN prior to MCAO or sham conditions did not result in any significant change in RVLM neuronal activity. These results indicate that estrogen receptors in the PBN play a major role in modulating the sympathoexcitatory response from ischemic forebrain nuclei, and that the pathway from the PBN to sympathetic preganglionic nuclei may not involve a synapse in the RVLM.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2005.10.062