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The Journal of Neurophysiology Vol. 82 No. 5 November 1999, pp. 2649-2656
Copyright ©1999 by the American Physiological Society
Department of Oral and Craniofacial Biological Sciences, University of Maryland Dental School, Baltimore, Maryland 21201
Andrew, David and
Joel D. Greenspan.
Mechanical and Heat Sensitization of Cutaneous Nociceptors After
Peripheral Inflammation in The Rat. J. Neurophysiol. 82: 2649-2656, 1999. Tissue injuries commonly
cause an increase in pain sensitivity, so that normally painful stimuli
become more painful (hyperalgesia), and those usually associated with
nonnoxious sensations evoke pain (allodynia). The neural bases for
these sensory phenomena have been explored most extensively using heat
injuries and experimental arthritis as models. Heat sensitization of
cutaneous nociceptors is observed after burns, and sensitization of
articular afferents to limb movements occurs after knee joint
inflammation. These are likely to be peripheral mechanisms of
hyperalgesia. Others, using different models of peripheral
inflammation, have only rarely found mechanical sensitization of
cutaneous nociceptors. In general these studies have failed to evaluate
suprathreshold mechanical sensitivity, which has led to the concept
of enhanced spinal cord processing ("central sensitization")
serving as the neural substrate for mechanical hyperalgesia. In the
current experiments, the mechanical and heat responses of cutaneous
nociceptors supplying the glabrous skin of the rat hindpaw were studied
16-24 h after induction of acute inflammation with complete Freund's
adjuvant. Single-fiber recordings were made from nociceptors in the
sciatic nerve of barbiturate-anesthetized animals, and their responses
compared with those obtained from nociceptors tested identically in
normal animals. Nociceptors were characterized by the following:
1) graded mechanical stimuli (5-90 g) delivered with
probes of tip area of 1 and 0.1 mm2, 2)
their adaptive responses to 2-min mechanical stimuli at three intensities, and 3) their responses to graded heat
stimuli (40-50°C). Forty-three nociceptors were studied in the
inflamed state; 20 were A fibers, and the remainder were C fibers.
Mechanical thresholds, determined with calibrated monofilaments, were
not significantly different from controls. Sensitization to
suprathreshold mechanical stimuli was observed for both A- and C-fiber
nociceptors, although it was greater for the A fibers. Similarly,
sensitization during testing of adaptive properties of A- and C-fiber
nociceptors was seen, although it was limited to the dynamic (initial)
and not the static (plateau) phase of the response. Heat sensitization was observed in 25% of A-fiber nociceptors, but the responses of C
fibers to heat were depressed. Other indicators of neuronal sensitization, such as spontaneous activity and expanded receptive fields, were also observed. It was concluded that the mechanical hyperalgesia caused by peripheral inflammation could be explained by
nociceptor sensitization. Central mechanisms cannot be completely ruled
out as contributing to such hyperalgesia, although their role may be
much smaller than previously envisaged.
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