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Received September 19, 2001
Accepted after revision October 31, 2001
1 Indiana University School of Medicine, Program in Medical Neurobiology, Indianapolis, IN 46202, USA
2 Indiana University School of Medicine, Department of Pharmacology and Toxicology, Indianapolis, IN 46202, USA
3 Indiana University School of Medicine, Department of Pharmacology and Toxicology, 635 Barnhill Drive, Room MS A421, Indianapolis, IN 46202, USA
* To whom correspondence should be addressed. E-mail: jdimicco{at}iupui.edu.
Activation of neurons in the region of the dorsomedial hypothalamus (DMH) appears to generate the sympathetically mediated tachycardia seen in experimental air stress in rats. The purpose of this study was to assess the role of neurons in the area of the medullary raphe pallidus (RP) in the tachycardia caused by stimulation of the DMH. The cardiovascular response to microinjection of the GABAA receptor antagonist bicuculline methiodide (BMI) 10 pmol (100 nl)-1 into the DMH was assessed before, and after, injection of the GABAA receptor agonist muscimol 80 pmol (100 nl)-1 or saline vehicle 100 nl into the RP in urethane-anaesthetized rats. Tachycardia evoked by microinjection of BMI into the DMH was mimicked by microinjection of BMI 30 pmol (75 nl)-1 into the RP. This DMH-induced tachycardia was markedly suppressed after injection of muscimol into the RP, but the response was unaffected by injection of saline into the same region. Thus, DMH-induced tachycardia is mediated through activation of neurons in the area of the RP, suggesting that these neurons may play a previously unrecognized role in stress-induced cardiac stimulation.
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