Literature DB >> 2388073

Evidence for a central component in the sensitization of spinal neurons with joint input during development of acute arthritis in cat's knee.

V Neugebauer1, H G Schaible.   

Abstract

1. In the spinalized cat, nociceptive spinal neurons with knee input show enhanced responses to mechanical stimulation of that joint once an inflammation has developed in the knee. Enhanced responses may result from increased afferent inflow as well as from modifications of the nociceptive processing within the spinal cord. To examine the significance of these components, we tested in 30 chloralose-anesthetized, spinalized cats whether, during development of arthritis, changes of responsiveness in spinal neurons are restricted to stimulation of the inflamed joint or whether responsiveness in these neurons is altered in general. While continuously recording from a neuron, we injected kaolin and carrageenan into one knee and tested the responses to mechanical stimuli applied to the joint and to regions adjacent to and remote from the knee during the developing arthritis. In addition, in six cats we monitored the neurons' responses to electrical stimulation of the sural nerves and the rostral lumbar spinal cord. 2. Of 32 neurons in laminae VI, VII, and VIII of the lumbar spinal cord, 15 ascending and eight nonascending cells were driven by mechanical stimulation of one or both knee joint(s). Nine of these were nociceptive specific (NS), responding exclusively or predominantly to noxious compression of the knee and other deep tissue, and 12 were wide-dynamic-range (WDR) cells with graded responses to gentle and noxious stimuli applied to the knee joint(s), deep tissue, and skin. Two neurons with high ongoing discharges had some excitatory joint input but showed marked inhibition by most stimuli used (INH neurons). The majority of the neurons had receptive fields on both legs. Nine of the 32 neurons had no input from the knee(s). 3. All 23 neurons with joint input became sensitive or more responsive to movements and gentle compression of the inflamed knee once the inflammation had developed. In general, these neurons also showed enhanced responses to compression of the adjacent muscles in thigh and lower leg. In 20 neurons, response properties were even altered for stimuli applied to regions remote from the inflamed joint, including the contralateral leg in 18 cases. We found expansion of initially restricted receptive fields (mainly in NS cells), enhancement of preexisting responses, and/or lowering of threshold to mechanical stimuli applied to these regions; few neurons developed inhibitory reactions.(ABSTRACT TRUNCATED AT 400 WORDS)

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Year:  1990        PMID: 2388073     DOI: 10.1152/jn.1990.64.1.299

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  28 in total

1.  Alteration of descending modulation of nociception during the course of monoarthritis in the rat.

Authors:  N Danziger; J Weil-Fugazza; D Le Bars; D Bouhassira
Journal:  J Neurosci       Date:  1999-03-15       Impact factor: 6.167

2.  Prevention and reversal of latent sensitization of dorsal horn neurons by glial blockers in a model of low back pain in male rats.

Authors:  Juanjuan Zhang; Siegfried Mense; Rolf-Detlef Treede; Ulrich Hoheisel
Journal:  J Neurophysiol       Date:  2017-06-14       Impact factor: 2.714

3.  Chapter 9 The dorsal horn and hyperalgesia.

Authors:  Karin N Westlund
Journal:  Handb Clin Neurol       Date:  2006

4.  Differential presynaptic control of the synaptic effectiveness of cutaneous afferents evidenced by effects produced by acute nerve section.

Authors:  P Rudomin; I Jiménez; D Chávez
Journal:  J Physiol       Date:  2013-03-11       Impact factor: 5.182

5.  Central Control of Peripheral Joint Inflammation and Heat Hyperalgesia.

Authors:  Kathleen A Sluka; William D Willis; Karin N Westlund
Journal:  Prog Pain Res Manag       Date:  1994-01-01

6.  Electrophysiological evidence for a spinal antinociceptive action of dipyrone.

Authors:  V Neugebauer; H G Schaible; X He; T Lücke; P Gündling; R F Schmidt
Journal:  Agents Actions       Date:  1994-03

7.  Spinal prostaglandins are involved in the development but not the maintenance of inflammation-induced spinal hyperexcitability.

Authors:  E Vasquez; K J Bär; A Ebersberger; B Klein; H Vanegas; H G Schaible
Journal:  J Neurosci       Date:  2001-11-15       Impact factor: 6.167

8.  Hemispheric lateralization of pain processing by amygdala neurons.

Authors:  Guangchen Ji; Volker Neugebauer
Journal:  J Neurophysiol       Date:  2009-07-22       Impact factor: 2.714

9.  Effect of RP 67580, a non-peptide neurokinin1 receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat.

Authors:  J M Laird; R J Hargreaves; R G Hill
Journal:  Br J Pharmacol       Date:  1993-07       Impact factor: 8.739

10.  Dynamic changes in the receptive field properties of spinal cord neurons with ankle input in rats with chronic unilateral inflammation in the ankle region.

Authors:  B D Grubb; R U Stiller; H G Schaible
Journal:  Exp Brain Res       Date:  1993       Impact factor: 1.972

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