This study used the expression of c-fos as a marker of
neuronal stimulation to determine whether decreased baroreceptor afferent
activity could activate PNMT-containing (C1) neurons.
Baroreceptor afferents were decreased using two treatments:
hydralazine injection (vasodilatoràhypotension)
or surgical denervation of the carotid sinus and aortic baroreceptors
(artificial hypotension). Control rats received saline injections or sham
denervation, respectively. Some rats received Fluorogold injections to
retrogradely label bulbospinal RVLM neurons. Finally, neurons were stained for
Fos, the protein produced by the c-fos gene. Separate groups of rats had
catheters placed in the right femoral artery to record MAP and heart rate in
response to hydralazine or sinoaortic denervation. Stained neurons were counted via light microscopy.
In hydralazine-injected rats, approximately 80% of the
PNMT-positive neurons in the RVLM were immunoreactive for Fos. This was true of
the entire population of PNMT-positive neurons as well as the specific group of
PNMT-positive neurons that were also labeled with Fluorogold. Approximately 45%
of the Fluorogold-positive neurons contained PNMT in the hydralazine- and
saline-injected groups. Approximately 40% of the PNMT-positive neurons were
also label with Fluorogold. If 80% of the spinally projecting C1 neurons are
affected by baroreceptor afferent input, and C1 neurons comprise 40% of the
bulbospinal RVLM neurons, then greater than one-third of the bulbospinal RVLM
neurons that are sensitive to baroreceptor afferent input must be C1 neurons. Neurons
in the RVLM express Fos in response to sinoaortic denervation as well as
hydralazine injection.
These results are central to a lot of the work we do in our
lab.
-BH
-BH
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