Diffuse noxious inhibitory controls (DNIC) in the rat with or without pCPA pretreatment

Dickenson, Anthony H.; Rivot, J.P.; Chaouch, Athmane; Besson, Jean‐Marie; Bars, D. Le

doi:10.1016/0006-8993(81)90133-5

Cited by 67 publications

(24 citation statements)

References 21 publications

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“…Since there are many inhibitory interneurons in the dorsal horn, the excitation produced by 5-HT on those inhibitory neurons may cause the dis-inhibition on the sensory transmission (78). The stimulation of the raphe magnus causes a inhibition of nociceptive dorsal horn neurons that seems to be mediated by the activation of the descending 5-HT systems since pretreatment of PCPA reduces the effect of raphe stimulation (79,80) As described above, 5-HT 3 receptors are expressed on small primary afferent fibers and the activation of these receptors may cause the release of glutamate onto the dorsal horn neurons. It is not known whether the interneurons that are activated by released glutamate are excitatory or inhibitory interneurons.…”

Section: Behavioral Studymentioning

confidence: 97%

Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

2006

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Abstract. The sensation of pain plays a critical role as an alert and as a protection system against tissue damage from mechanical, chemical, and thermal stimuli. Despite the protective role of pain, the severity of pain sensation is markedly attenuated by the endogenous pain inhibitory systems that predominantly originate at the brain stem. Both behavioral and in vivo extracellular recording studies have sought the loci producing analgesia and clarification of the anti-nociceptive actions. Among those loci, the main descending systems to the spinal dorsal horn are noradrenergic and serotonergic. Although, in vivo studies have provided basic knowledge of these systems, the precise synaptic mechanisms underlying the analgesic actions have not yet been elucidated until recently. The newly developed in vitro slice and in vivo patchclamp recordings have disclosed the synaptic mechanisms of the noradrenergic and serotonergic effects at the level of spinal dorsal horn. This paper reviews the anti-nociceptive action of these systems, while particularly focusing on the electrophysiological aspects of the systems at the single neuron level in the spinal dorsal horn as well as their origins and responsible receptor subtypes.

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Section: Behavioral Studymentioning

confidence: 97%

Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

2006

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“…Furthermore, manipulations of the descending serotoninergic projections from nucleus raphe magnus of the brain stem, the terminals of which synapse in the dorsal horn of the spinal cord (Skagerberg & Bjorklund, 1985) interfere with d.n.i.c. Hence lesions of the nucleus (Dickenson et al 1980b), section of the dorsolateral funiculus ) in which the descending fibres travel, depletion of serotonin (Dickenson, Rivot, Chaouch, Besson & Le Bars, 1981) and serotonin receptor antagonism (Chitour, Dickenson & Le Bars, 1982) all markedly reduce d.n.i.c. Since direct spinal projections from the 100 SUPRASPINAL MORPHINE p.a.g.…”

Section: Effects Of Morphine On the C-fibre Evoked Responsesmentioning

confidence: 99%

Supraspinal morphine and descending inhibitions acting on the dorsal horn of the rat.

Dickenson

Bars

1987

The Journal of Physiology

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SUMMARY1. Recordings were made from thirty-nine convergent neurones in the lumbar enlargement of the rat spinal cord. These neurones were activated by both innocuous and noxious stimuli applied to their excitatory receptive fields located on the extremity of the ipsilateral hind paw. Transcutaneous application of suprathreshold 2 ms square-wave pulses to the centre of the receptive field resulted in responses to A-and C-fibre activation being observed; a mean of 18-8+ 1-8 C-fibre latency spikes was evoked per stimulus. This type of response was inhibited by applying noxious conditioning stimuli to heterotopic body areas; immersing the tail in a 52°Cwater-bath caused a mean 54-5 + 2-3 % inhibition of the C-fibre-evoked response; such inhibitory processes have been termed diffuse noxious inhibitory controls (d.n.i.c.).2. The effects of microinjections of morphine (5 jig; Q-2 #1) on both the unconditioned C-fibre-evoked response and inhibitory processes triggered from the tail were investigated in an attempt to answer two questions: (a) does morphine increase tonic descending inhibitory processes and (b) 6. Autoradiographic controls using [3H]morphine showed a large diffusion of the drug within an area of about 0 75 mm around the tip of the cannula. Although the dose used (5,ug) was low, the mean concentration within the diffusion sphere was in the 10 mm range, far exceeding the concentrations reached following systemic doses of morphine.7. It is concluded that high concentrations of morphine within the p.a.g. do not increase tonic descending inhibitory controls but rather decrease them and yet clearly depress d.n.i.c. when the injection sites are within or close to the dorsal raphe nucleus. Since the time course of these effects is related to the behavioural analgesia induced by identical procedures, these findings are discussed with reference to the functional role of d.n.i.c. in pain processes.

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“…It follows then, that DNIC shares conceptual similarities with SIA and some models of SIA involve exposure to noxious stimuli followed by subsequent tests of responding to additional noxious stimuli (Table 1). DNIC, like SIA, has been demonstrated in rodents (Dickenson et al, 1981) and humans (Chen et al, 1985;Le Bars et al, 1992;Talbot et al, 1989).…”

Section: Diffuse Noxious Inhibitory Controlmentioning

confidence: 97%

“…By contrast a role for the caudal medullaspinal connectivity has been demonstrated (Bouhassira et al, 1995) and, lesions of subnucleus reticularis dorsalis in the caudal medulla strongly reduce DNIC (Bouhassira et al, 1992c). As with SIA, there is evidence for a role of the opioid (Bouhassira et al, 1988;Le Bars et al, 1987;Willer et al, 1990) and serotonergic systems (Dickenson et al, 1981) in DNIC. Thus, while these two forms of endogenous analgesia can be separated neuroanatomically, there may be a degree of convergence at the level of neurotransmitters/neuropeptides.…”

Section: Diffuse Noxious Inhibitory Controlmentioning

confidence: 99%

“…Diffuse noxious inhibitory control (DNIC) describes the strong inhibition of neurons in the dorsal horn of the spinal cord when a nociceptive stimulus is applied to any part of the body, distinct from their excitatory receptive fields (Dickenson et al, 1981; for review see Villanueva and Le Bars, 1995). DNIC manifests as a decrease in pain sensation to a noxious stimulus applied to one part of the body during or following application of another noxious stimulus to a different part of the body.…”

Section: Diffuse Noxious Inhibitory Controlmentioning

confidence: 99%

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Stress-Induced Analgesia

Tricklebank¹,

Curzon²

2013

Encyclopedia of Pain

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Abbreviations: SIA, stress-induced analgesia; FCA, fear-conditioned analgesia; GABA, Ȗ-aminobutyric acid; HA, high analgesia; LA, low analgesia; fMRI, functional magnetic resonance imaging; DNIC, diffuse noxious inhibitory control; PAG, periaqueductal grey; RVM, rostroventral medulla; 5-HT, 5-hydroxytryptamine; CB 1 , cannabinoid type 1; CB 2 , cannabinoid type 2; NMDA, N-methyl-D-aspartic acid; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; mGluR, metabotropic glutamate receptor; NK1, neurokinin 1; SP, substance P; 2-AG, 2-arachidonoylglycerol; FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; HPA, hypothalamo-pituitary-adrenal; ACTH, adrenocorticotropic hormone 3 ABSTRACT For over 30 years, scientists have been investigating the phenomenon of pain suppression upon exposure to unconditioned or conditioned stressful stimuli, commonly known as stress-induced analgesia. These studies have revealed that individual sensitivity to stressinduced analgesia can vary greatly and that this sensitivity is coupled to many different phenotypes including the degree of opioid sensitivity and startle response. Furthermore, stress-induced analgesia sensitivity can vary a great deal depending on age, gender, and prior experience to stressful, painful, or other environmental stimuli. Stress-induced analgesia is mediated by activation of the descending inhibitory pain pathway.Pharmacological and neurochemical studies have demonstrated involvement of a large number of neurotransmitters and neuropeptides. In particular, there are key roles for the HQGRJHQRXV RSLRLG PRQRDPLQH FDQQDELQRLG Ȗ-aminobutyric acid and glutamate systems. The study of stress-induced analgesia has enhanced our understanding of the fundamental physiology of pain and stress and has been a useful approach for uncovering new therapeutic targets for the treatment of pain and stress-related disorders.4

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Diffuse noxious inhibitory controls (DNIC) in the rat with or without pCPA pretreatment

Cited by 67 publications

References 21 publications

Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

Supraspinal morphine and descending inhibitions acting on the dorsal horn of the rat.

Stress-Induced Analgesia

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