Spinal mechanisms underlying persistent pain and referred hyperalgesia in
rats with an experimental ureteric stone.
Carolina ROZA, Jennifer M.A. LAIRD & Fernando CERVERO.
Department of Physiology, Faculty of Medicine, University of Alcal ,
Alcal de Henares, E-28871 Madrid, Spain.
APStracts 4:341N, 1997.
ABSTRACT
Spinal neurons processing information from the ureter have been characterized
in rats one to four days after the implantation of an experimental ureteric
stone and compared with those of normal rats. The effects of a conditioning
noxious stimulation of the ureter in the presence of the hyperalgesia evoked
by the calculosis were also examined.
Extracellular recordings were performed at the T12-L1 segments of the spinal
cord. In rats with calculosis more neurons expressed a ureter input (53% vs
42% in normal rats); such cells being more likely to show background activity,
at a higher rate than normals (6.6 ñ 1.2 spikes/s vs 3.2 ñ 0.9) and increasing
with the continuing presence of the stone. The threshold pressure for a
ureteric response was higher than in normal rats (79 ñ 5 mmHg vs 54 ñ 4) but
the neurons failed to encode increasing intensities of stimulation. Thirty-
five percent of the neurons with exclusively innocuous somatic receptive
fields had a ureter input in rats with calculosis whereas none were seen in
normal rats. A noxious ureteric distention applied to neurons with ureter
input evoked a complex mixture of increases and decreases in somatic receptive
field size and/or somatic input properties markedly different from the
generalized increases in excitability seen when such a stimulus was applied to
normal animals.
We conclude that the presence of a ureteric stone evokes excitability changes
of spinal neurons (enhanced background activity, greater number of ureter-
driven cells, decreased threshold of convergent somatic receptive fields)
which likely account for the referred hyperalgesia seen in rats with
calculosis. However, further noxious visceral input occurring in the presence
of persistent hyperalgesia produces selective changes that cannot be explained
by a generalized excitability increase and suggest that the mechanisms
underlying maintenance of hyperalgesia include alteration of both central
inhibitory and excitatory systems.
Received 18 September 1997; accepted in final form 25 November 1997.
APS Manuscript Number J771-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 12 December 1997