Dorsal horn administration of muscimol abolishes the muscle pressor reflex

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 GABA(A) agonist muscimol to the dorsal surface of the spinal cord. Cats were anesthetized with alpha-chloralose and urethane, and a laminectomy was performed. With the exception of the L(7) dorsal root, the dorsal and ventral roots from L(5) to S(2) were sectioned on one side, and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L(7) and S(1) ventral roots. The dorsal surface of the L(4)--S(3) 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 L(7) 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.