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1 Department of Neuroscience, University of Pittsburgh, Pittsburg, USA
* To whom correspondence should be addressed. E-mail: sved{at}bns.pitt.edu.
To evaluate the role of C1 neurons in the rostral ventrolateral medulla (RVLM) in cardiovascular regulation, we studied rats in which this cell group was destroyed by injection of anti-dopamine-
-hydroxylase-saporin into the RVLM. These immunotoxin injections resulted in 32-99% depletions of the RVLM-C1 neurons, and ~50% depletions of the A5 cell population. In conscious rats with large (>80%) depletions of the RVLM-C1 cell population resting arterial pressure was approximately 10 mm Hg lower than in control injected rats, though heart rate was not significantly different. Similar results were observed when arterial pressure was recorded in urethan-anesthetized rats, though under anesthesia heart rate was also reduced in rats with large (>80%) depletions of the RVLM-C1 neuronal population. Sympathoexcitatory responses to baroreceptor unloading, chemoreceptor activation, and electrical stimulation of sciatic nerve afferent fibers were attenuated in rats with >80% depletions of the RVLM-C1 cell population. These effects of RVLM-C1 plus A5 cell populations were not mimicked by either smaller lesions of the RVLM-C1 population or by selective destruction of the A5 cell population with 6-hydroxydopamine. Sympathoinhibitory responses such as decreases in arterial pressure and heart rate evoked by injection of GABA into the RVLM or by intravenous phenylbiguanide administration were not altered by RVLM-C1 plus A5 cell depletion. These data suggest that RVLM-C1 cells contribute to the maintenance of baseline arterial pressure and play an integral role in sympathoexcitatory responses.
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