The paraventricular nucleus (PVN), a cell
group located bilaterally along the third
ventricle, regulates neuroendocrine and
cardiovascular functions, and modulates
sympathetic outflow. Because many stimuli that
influence sympathetic activity also affect
breathing, it might be expected that stimulation
of the PVN would change ventilation. Hence, the
aim of this study was, first to examine whether
activation of PVN neurons results in changes in
respiratory output and pattern of breathing, and
second to determine the connections between PVN
and phrenic motoneurons through which PVN
neurons might influence respiration.
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The present study indicates that PVN can
exert excitatory influences on respiratory
drive. This effect can be mediated through
PVN-brainstem and/or PVN-spinal cord pathways.
In a previous study using the retrograde
transneuronal marker, pseudorabies virus (PRV),
we had shown that PVN was consistently labeled
when the PRV was injected into the right
hemidiaphragm of C8-T1 spinalectomized rats
after ipsilateral cervical vagotomy, or in
phrenic nerve. Because, PRV infects also the
second order neurons, the results of the present
study indicate the presence of direct projection
from PVN to the phrenic motoneurons, and extend
earlier studies related to connectivity of PVN
with brainstem and spinal cord autonomic
nuclei.
Physiologically, the present study
demonstrated for the first time that activation
of the PVN significantly influenced the
magnitude of DEmG and the respiratory timing,
which could be mediated by two pathways: (1)
through the brainstem bulbospinal and, (2)
probably via the direct connection with phrenic
nucleus.
Although there are few physiological studies
relating activation of PVN and respiration,
Ferguson et al. have indirectly inferred through
electrical stimulation of the subfornical organ
that the changes in the respiratory pattern
observed were mediated through the medullary
center via the PVN. The relatively long changes
in respiratory pattern observed following the
injection of L-glutamate into PVN could be
attributed to PVN's projection (possibly through
vasopressin and oxytocin), to brainstem
respiratory related cells, and to phrenic
motoneurons.
In summary, the results of this study
indicate that the changes in breathing activity
associated with activation of the PVN neurons
are part of complex responses as a consequence
of activation of a network controlling
autonomic, neuroendocrine, cardiovascular, and
respiratory functions.