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Department of Physiology, University of South Alabama College of Medicine, Mobile, Alabama 36688
The purpose of this study was to determine the effect
of blocking synaptic transmission in the dorsal horn on the
cardiovascular responses produced by activation of muscle afferent
neurons. Synaptic transmission was blocked by applying the
GABAA agonist muscimol to the dorsal surface of the spinal
cord. Cats were anesthetized with 
-chloralose and urethane, and a
laminectomy was performed. With the exception of the L7
dorsal root, the dorsal and ventral roots from L5 to
S2 were sectioned on one side, and static contraction of
the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L7 and
S1 ventral roots. The dorsal surface of the
L4-S3 segments of the spinal cord were enclosed within a "well" created by applying layers of vinyl
polysiloxane. Administration of a 1 mM solution of muscimol (based on
dose-response data) into this well abolished the reflex pressor
response to contraction (change in mean arterial blood pressure before
was 47 ± 7 mmHg and after muscimol was 3 ± 2 mmHg). Muscle
stretch increased mean arterial blood pressure by 30 ± 8 mmHg
before muscimol, but after drug application stretch increased MAP by
only 3 ± 2 mmHg. Limiting muscimol to the L7 segment
attenuated the pressor responses to contraction (37 ± 7 to
24 ± 11 mmHg) and stretch (28 ± 2 to 16 ± 8 mmHg).
These data suggest that the dorsal horn of the spinal cord contains an
obligatory synapse for the pressor reflex. Furthermore, these data
support the hypothesis that branches of primary afferent neurons, not
intraspinal pathways, are responsible for the multisegmental
integration of the pressor reflex.
spinal cord; cardiovascular; cats; 
-aminobutyric acid
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