Behavioral confirmation of “diffuse noxious inhibitory controls” (DNIC) and evidence for a role of endogenous opiates

Kraus, E; Bars, D. Le; Besson, Jean‐Marie

doi:10.1016/0006-8993(81)90554-0

Cited by 60 publications

(14 citation statements)

References 8 publications

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“…The study's demonstration of the involvement of opioid peptides in endogenous analgesia is consistent with other animal (Kraus et al, 1981; Le Bars et al, 1981) studies of DNIC and CPM, respectively. Psychophysical tests like the cold pressor elicit β -endorphin release (Casale et al, 1985; Suzuki et al, 2007); which may bind to mu-opioid receptors in the central nervous system thereby reducing pain (Rosa et al, 1988; Suzuki et al, 2007).…”

Section: Discussionsupporting

confidence: 87%

“…Pharmacological studies have suggested a role of endogenous opioids through receptor blockade studies. Several animal studies have shown that opioid antagonists block the expression of stress-induced analgesia (Kelly & Franklin, 1987; King et al, 2007; Tricklebank et al, 1984) and DNIC (Kraus et al, 1981; Le Bars et al, 1981). In human studies of CPM (Table 1), however, the role of opioid peptides in endogenous analgesia has been inconsistent with some studies reporting blockade of pain inhibition (Pertovaara et al, 1982; Willer et al, 1990) while others report that opioid antagonists failed to affect inhibition (Edwards et al, 2004; Peters et al, 1992; Sprenger et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Reduction of conditioned pain modulation in humans by naltrexone: an exploratory study of the effects of pain catastrophizing

et al. 2012

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The current study tested the hypothesis that conditioned pain modulation is mediated by the release of endogenous opioids with a placebo-controlled (sugar pill) study of naltrexone (50 mg) in 33 healthy volunteers over two counter-balanced sessions. Pain modulation consisted of rating of heat pain (palm) during concurrent cold water immersion (foot). Compared to baseline heat pain ratings, concurrent foot immersion lowered pain intensity ratings, which suggests an inhibitory effect, was reduced with naltrexone, suggesting at least partial dependence of inhibition on endogenous opioids. An exploratory analysis revealed that individual differences in catastrophizing moderated the effects of naltrexone; endogenous opioid blockade abolished modulation in subjects lower in catastrophizing while modulation was unaffected by naltrexone among high catastrophizers. The results suggest a role of endogenous opioids in endogenous analgesia, but hint that multiple systems might contribute to conditioned pain modulation, and that these systems might be differentially activated as a function of individual differences in responses to pain.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Reduction of conditioned pain modulation in humans by naltrexone: an exploratory study of the effects of pain catastrophizing

et al. 2012

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“…Visceral pain induced by i.p. injection of phenylbenzoquinone inhibited vocalization induced by electrical stimuli applied to the tail, and this inhibition was also dose-dependently reversed by systemic naloxone (127). Observations that DNIC was diminished by electrolytic lesion (128) or lidocaine microinjection (129) of the nucleus raphe magnus suggested that there is a contribution from this site to DNIC.…”

Section: Diffuse Noxious Inhibitory Controls Modulation Of Painmentioning

confidence: 99%

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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“…Diffuse noxious inhibitory controls are a unique form of endogenous analgesia, partly opioid, 18 in which the activity of trigeminal and spinal convergent wide-dynamic-range (WDR) neurons is inhibited through descending pathways. 21 In terms of descending modulation of the spinal cord, important pathways involve the dorsolateral funiculus comprising the periaqueductal grey, locus coeruleus (LC), and rostral ventromedial medulla (RVM) projections to the spinal cord.…”

Section: Introductionmentioning

confidence: 99%

Diffuse noxious inhibitory controls and nerve injury

Bannister

Patel²,

Gonçalves³

et al. 2015

Pain

148

115

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Diffuse noxious inhibitory controls (DNICs) utilize descending inhibitory controls through poorly understood brain stem pathways. The human counterpart, conditioned pain modulation, is reduced in patients with neuropathy aligned with animal data showing a loss of descending inhibitory noradrenaline controls together with a gain of 5-HT3 receptor-mediated facilitations after neuropathy. We investigated the pharmacological basis of DNIC and whether it can be restored after neuropathy. Deep dorsal horn neurons were activated by von Frey filaments applied to the hind paw, and DNIC was induced by a pinch applied to the ear in isoflurane-anaesthetized animals. Spinal nerve ligation was the model of neuropathy. Diffuse noxious inhibitory control was present in control rats but abolished after neuropathy. α2 adrenoceptor mechanisms underlie DNIC because the antagonists, yohimbine and atipamezole, markedly attenuated this descending inhibition. We restored DNIC in spinal nerve ligated animals by blocking 5-HT3 descending facilitations with the antagonist ondansetron or by enhancing norepinephrine modulation through the use of reboxetine (a norepinephrine reuptake inhibitor, NRI) or tapentadol (μ-opioid receptor agonist and NRI). Additionally, ondansetron enhanced DNIC in normal animals. Diffuse noxious inhibitory controls are reduced after peripheral nerve injury illustrating the central impact of neuropathy, leading to an imbalance in descending excitations and inhibitions. Underlying noradrenergic mechanisms explain the relationship between conditioned pain modulation and the use of tapentadol and duloxetine (a serotonin, NRI) in patients. We suggest that pharmacological strategies through manipulation of the monoamine system could be used to enhance DNIC in patients by blocking descending facilitations with ondansetron or enhancing norepinephrine inhibitions, so possibly reducing chronic pain.

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Behavioral confirmation of “diffuse noxious inhibitory controls” (DNIC) and evidence for a role of endogenous opiates

Cited by 60 publications

References 8 publications

Reduction of conditioned pain modulation in humans by naltrexone: an exploratory study of the effects of pain catastrophizing

Reduction of conditioned pain modulation in humans by naltrexone: an exploratory study of the effects of pain catastrophizing

Central modulation of pain

Diffuse noxious inhibitory controls and nerve injury

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