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Vagal
inhibition of thoracic neurons
As previously
discussed, excitation of cardiac sympathetic afferents excites
neurons in the upper thoracic and upper cervical segments, but
has little effect on neurons in the cervical enlargement. In addition,
excitation of vagal afferents excites neurons in the upper cervical
segments, but usually inhibits neurons in the upper thoracic segments.
Thus, the physiological responses of these neurons are well-described.
What are the
specific anatomical pathways within the brain stem and spinal
cord that mediate these responses, and what are the neurophysiological
mechanisms that can ultimately explain the sensations associated
with angina pectoris? There remain far more questions than answers
regarding the spinal mechanisms of these responses, but there
are some intriguing recent developments.
At least a
portion of the vagal inhibitory effects on thoracic neurons may
depend on a relay through the C1-C2 segments (Figure
7).
Destruction
of C1-C2 neurons, but not axons passing through this area, with
the excitotoxin ibotenic acid eliminates the inhibitory effects
of vagal stimulation on thoracic spinal neurons. Intrapericardial
injections of chemicals analogous to those released by the heart
during ischemia excite thoracic neurons, and this excitation is
attenuated by vagal stimulation. This suppressor effect of vagal
stimulation is prevented by application of ibotenic acid to the
upper cervical spinal cord.
These pieces
of evidence suggest that there is a propriospinal pathway with
cell bodies in the C1-C2 region and axons terminating in the upper
thoracic spinal cord that participates in vagal inhibition of
thoracic spinal neurons.
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