Facilitation and attenuation of a visceral nociceptive reflex from the rostroventral medulla in the rat

M Zhuo, GF Gebhart - Gastroenterology, 2002 - Elsevier
Gastroenterology, 2002Elsevier
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 …
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 μA) and inhibiting it at greater (>50 μA) intensities of stimulation. Electrical stimulation at all intensities tested (5200 μA) 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.
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