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1 Department of Physiology and Institute for Biomedical Research, University of Sydney, Sydney, NSW, Australia
2 University of Melbourne, Neurobiology Group, Howard Florey Institute, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: rogerd{at}physiol.usyd.edu.au.
The dorsomedial hypothalamic nucleus (DMH) is believed to play a key role in mediating vasomotor and cardiac responses evoked by an acute stress. Inhibition of neurons in the rostral ventrolateral medulla (RVLM) greatly reduces the increase in renal sympathetic nerve activity (RSNA) evoked by activation of the DMH, indicating that RVLM neurons mediate, at least in part, the vasomotor component of the DMH-evoked response. In this study, the first aim was to determine whether neurons in the medullary raphe pallidus (RP) region also contribute to the DMH-evoked vasomotor response, because it has been shown that the DMHevoked tachycardia is mediated by the RP region. The second aim was to assess directly the effect of DMH activation on the firing rate of RVLM sympathetic premotor neurons. In urethane-anesthetized rats, injection of the GABAA receptor agonist muscimol (but not vehicle solution) into the RP region caused a modest (~25%) but significant reduction in the increase in RSNA evoked by DMH disinhibition (by microinjection of bicuculline). In other experiments, disinhibition of the DMH resulted in a powerful excitation (increase in firing rate of ~400%) of 5 out of 6 spinally-projecting barosensitive neurons in the RVLM. The results indicate that neurons in the RP region make a modest contribution to the renal sympathoexcitatory response evoked from the DMH, and also that sympathetic premotor neurons in the RVLM receive strong excitatory inputs from DMH neurons, consistent with the view that the RVLM plays a key role in mediating sympathetic vasomotor responses arising from the DMH.
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