Min Zhuo1, G F Gebhart. 1. Department of Pharmacology, College of Medicine, The University of Iowa, Iowa City, Iowa 52242, USA.
Abstract
BACKGROUND & AIMS: Noxious inputs from somatic tissue are subject to biphasic descending modulation from the rostroventral medulla (RVM). In the present study, we investigated descending facilitatory and inhibitory influences from the RVM on a visceral nociceptive reflex. METHODS: The visceromotor response (VMR), a contraction of peritoneal musculature during noxious colorectal distention (80 mm Hg, 20 seconds), was quantified as the integrated electromyogram. RESULTS: At 22 sites in the RVM, electrical stimulation produced biphasic effects, facilitating the VMR at low (5, 10, and 25 microA) and inhibiting it at greater (>50 microA) intensities of stimulation. Electrical stimulation at all intensities tested (5-200 microA) in other sites in the RVM only inhibited (30 sites) or only facilitated (12 sites) the VMR to colorectal distention. Activation of glutamatergic receptors in the RVM replicated the effects of electrical stimulation. Reversible blockage (intraspinal lidocaine injection) or irreversible transection of spinal funiculi revealed that descending facilitatory influences from the RVM were conveyed in the ventrolateral/ventral funiculus, whereas descending inhibitory influences were contained in the dorsolateral funiculi. CONCLUSIONS: Spinal visceral nociceptive reflexes are subject to facilitatory modulation from the RVM, providing the basis for a mechanism by which visceral sensations can be enhanced from supraspinal sites.
BACKGROUND & AIMS: Noxious inputs from somatic tissue are subject to biphasic descending modulation from the rostroventral medulla (RVM). In the present study, we investigated descending facilitatory and inhibitory influences from the RVM on a visceral nociceptive reflex. METHODS: The visceromotor response (VMR), a contraction of peritoneal musculature during noxious colorectal distention (80 mm Hg, 20 seconds), was quantified as the integrated electromyogram. RESULTS: At 22 sites in the RVM, electrical stimulation produced biphasic effects, facilitating the VMR at low (5, 10, and 25 microA) and inhibiting it at greater (>50 microA) intensities of stimulation. Electrical stimulation at all intensities tested (5-200 microA) in other sites in the RVM only inhibited (30 sites) or only facilitated (12 sites) the VMR to colorectal distention. Activation of glutamatergic receptors in the RVM replicated the effects of electrical stimulation. Reversible blockage (intraspinal lidocaine injection) or irreversible transection of spinal funiculi revealed that descending facilitatory influences from the RVM were conveyed in the ventrolateral/ventral funiculus, whereas descending inhibitory influences were contained in the dorsolateral funiculi. CONCLUSIONS: Spinal visceral nociceptive reflexes are subject to facilitatory modulation from the RVM, providing the basis for a mechanism by which visceral sensations can be enhanced from supraspinal sites.