Effect of naloxone upon diffuse noxious inhibitory controls (DNIC) in the rat

Bars, D. Le; Chitour, Djamel; Kraus, E; Dickenson, Anthony H.; Besson, J. M.

doi:10.1016/0006-8993(81)90597-7

Cited by 123 publications

(46 citation statements)

References 89 publications

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“…Importantly, DNIC was not demonstrated in dorsal horn units that responded solely to noxious, proprioceptive, or innocuous inputs, indicating a requirement for convergent neurons receiving both noxious and innocuous stimuli (125). In addition, DNIC was abolished by spinal cord section and was diminished by systemic naloxone administration (124)(125)(126). Visceral pain induced by i.p.…”

Section: Diffuse Noxious Inhibitory Controls Modulation Of Painmentioning

confidence: 97%

Central modulation of pain

Ossipov¹,

Dussor²,

Porreca³

2010

J. Clin. Invest.

908

728

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It has long been appreciated that the experience of pain is highly variable between individuals. Pain results from activation of sensory receptors specialized to detect actual or impending tissue damage (i.e., nociceptors). However, a direct correlation between activation of nociceptors and the sensory experience of pain is not always apparent. Even in cases in which the severity of injury appears similar, individual pain experiences may vary dramatically. Emotional state, degree of anxiety, attention and distraction, past experiences, memories, and many other factors can either enhance or diminish the pain experience. Here, we review evidence for "top-down" modulatory circuits that profoundly change the sensory experience of pain.

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Section: Diffuse Noxious Inhibitory Controls Modulation Of Painmentioning

confidence: 97%

Central modulation of pain

Ossipov¹,

Dussor²,

Porreca³

2010

J. Clin. Invest.

908

728

View full text Add to dashboard Cite

show abstract

“…Secondly, age related changes in the neurophysiology of nociception and the perceptual experience of pain have been reported, including the reduced efficacy of the endogenous analgesic system in older people 24 . The diffuse noxious inhibitory control (DNIC) is a pain modulating process controlled by endogenous opioids which works via descending inhibition such that a noxious stimulus in one part of the body inhibits perception of a second painful stimulus [25][26][27][28] . Studies utilising experimental pain models on humans have reported age-related differences in this process whereby a first pain fails to modify a second pain, but instead enhances it [29][30][31] .…”

Section: Pain Mechanisms In People With Frailtymentioning

confidence: 99%

Pain in older people with frailty

Brown

Young

Clegg

et al. 2015

Rev. Clin. Gerontol.

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In this review we identified cohort and cross-sectional studies which assessed pain in community-dwelling older people (> 65 years) reliably characterised as frail. Secondly, we considered biologically plausible mechanisms which may alter pain perception, or contribute to, or exacerbate pain in an older person with frailty. Thirdly, we considered specific implications of pain management for this group of people. From the limited data from the seven included studies, it would appear that the presence of pain is higher in older people with frailty compared to people characterised as pre-frail or not frail. Thus, older people reporting pain are more likely to be frail. However, a lack of prospective data precludes inferences about the direction of the relationship: that is whether pain or frailty is the antecedent. Further research is needed to understand the direction of the relationship, and to identify appropriate pain management strategies for older people with frailty.

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“…Naloxone has been shown to enhance electrically evoked reflexes to impulses both in large-diameter muscle afferents and in large-and small-diameter cutaneous afferents (Duggan, Morton, Johnson & Zhao, 1984;Bell, Sharpe & Pickworth, 1985;Clarke & Ford, 1987, and for a review see Duggan & North, 1984). In most studies carried out in the dorsal horn, naloxone enhanced the afferent C fibre-evoked discharge of cells in laminae IV and V (Rivot, Chaouch & Besson, 1979;Fitzgerald & Woolf, 1980; LeBars, Chitour, Kraus, Dickenson & Besson, 1981); it does not, however, always do so . The effects of naloxone on the AS-evoked discharge were less clearly defined (Fitzgerald & Woolf, 1980) and no effects were observed on the Aa-evoked discharge (LeBars et al 1981).…”

Section: Introductionmentioning

confidence: 99%

“…In most studies carried out in the dorsal horn, naloxone enhanced the afferent C fibre-evoked discharge of cells in laminae IV and V (Rivot, Chaouch & Besson, 1979;Fitzgerald & Woolf, 1980; LeBars, Chitour, Kraus, Dickenson & Besson, 1981); it does not, however, always do so . The effects of naloxone on the AS-evoked discharge were less clearly defined (Fitzgerald & Woolf, 1980) and no effects were observed on the Aa-evoked discharge (LeBars et al 1981).…”

Section: Introductionmentioning

confidence: 99%

The effect of naloxone on spinal reflexes to electrical and mechanical stimuli in the anaesthetized, spinalized rat.

Hartell

Headley

1991

The Journal of Physiology

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SUMMARY1. Previous studies of the effects of naloxone on spinal neural responses have yielded disparate results. The reasons for this remain unclear but may relate to the diversity of animal preparations used, the route of administration of naloxone, the site and modality of the stimuli and the intensity of afferent input used. 2. A model requiring little preparative surgery compared to most other electrophysiological preparations has now been used to investigate the effects of naloxone (1, 10, 20 and 50 jug kg-l i.v.) on single-motor-unit flexion reflex responses to alternating mechanical and electrical stimuli in spinalized rats, anaesthetized with ac-chloralose.3. Naloxone caused a dose-dependent facilitation of reflex responses to electrical stimuli delivered at intensities sufficient to activate either A fibres alone or A and C fibre afferents together. The component of the responses presumed to be due primarily to activation of C fibres was enhanced relatively more than the A fibre component.4. Responses evoked during high-intensity mechanical pinch stimuli were not facilitated by equivalent doses of naloxone. The post-stimulus after-discharge was, however, enhanced by a similar percentage to the response to high-intensity electrical stimuli.5. Lowering the intensity of the mechanical stimulus led to a diminished firing rate of the units during the stimulus itself. The stimulus was, nevertheless, still noxious. Naloxone was found to have a facilitatory effect on this smaller evoked response both during the pinch stimulus and during the period of after-discharge. The apparent lack of effect of naloxone during the higher intensity mechanical stimulus may be due to neurones in the polysynaptic pathway being activated at near-maximal firing rates.6. We conclude that the ability of naloxone to facilitate spinal reflexes is not dependent on the nature of the stimulus, at least between electrical and mechanical stimuli, but is more a function of the intensity of the applied stimulus. MS 903217 PHY 442

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Effect of naloxone upon diffuse noxious inhibitory controls (DNIC) in the rat

Cited by 123 publications

References 89 publications

Central modulation of pain

Central modulation of pain

Pain in older people with frailty

The effect of naloxone on spinal reflexes to electrical and mechanical stimuli in the anaesthetized, spinalized rat.

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