Involvement of the subnucleus reticularis dorsalis in diffuse noxious inhibitory controls in the rat

Bouhassira, Didier; Villanueva, Luis; Zhu, Bing; Bars, D. Le

doi:10.1016/0006-8993(92)91071-l

Cited by 176 publications

(126 citation statements)

References 20 publications

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“…However, although the PAG can modulate counterirritation effects (Bouhassira et al, 1992b), it is not directly involved in DNIC (Bouhassira et al, 1990). Instead, DNIC is thought to mediate counterirritation effects on spinal nociceptive processes by the recruitment of the caudal medulla (De Broucker et al, 1990;Bouhassira et al, 1992a). The caudal medulla was not activated in the present study, but the absence of significant modulation of RIII in a subgroup of participants may have contributed to this negative result.…”

Section: Modulation Of Spinal Nociception By Counterirritationcontrasting

confidence: 53%

Cerebral and Cerebrospinal Processes Underlying Counterirritation Analgesia

Piché

Arsenault²,

Rainville³

2009

J. Neurosci.

146

112

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Pain is a complex experience involving extensive interactions between brain and spinal cord processes. Various interventions that modulate pain, such as the application of a competing noxious stimulus (counterirritation), are thought to involve cerebrospinal regulation through diffuse noxious inhibitory controls (DNICs). However, no study has yet examined the relation between brain and spinal cord activity during counterirritation analgesia in humans. This fMRI study investigates brain responses to phasic painful electrical stimulation administered to the sural nerve to evoke a spinal nociceptive response (RIII reflex) before, during and after counterirritation induced by the immersion of the left contralateral foot in cold water. Responses are compared with a control condition without counterirritation. As expected, counterirritation produced robust pain inhibition with residual analgesia persisting during the recovery period. In contrast, RIII reflex amplitude was significantly decreased by counterirritation only in a subset of subjects. Modulatory effects of counterirritation on pain perception and spinal nociception were paralleled by decreased shock-evoked activity in pain-related areas. Individual changes in shock-evoked brain activity were specifically related to analgesia in primary somatosensory cortex (SI), anterior cingulate cortex and amygdala, and to RIII modulation in supplementary motor area and orbitofrontal cortex (OFC). Moreover, sustained activation induced by the counterirritation stimulus in the OFC predicted shock-pain decrease while sustained activity in SI and the periaqueductal gray matter predicted RIII modulation. These results provide evidence for the implication of at least two partly separable neural mechanisms underlying the effects of counterirritation on pain and spinal nociception in humans.

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Section: Modulation Of Spinal Nociception By Counterirritationcontrasting

confidence: 53%

Cerebral and Cerebrospinal Processes Underlying Counterirritation Analgesia

Piché

Arsenault²,

Rainville³

2009

J. Neurosci.

146

112

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“…For example, lesions of the midbrain periaqueductal grey (PAG) (Bouhassira et al, 1992b), rostral ventromedial medulla (RVM) (Bouhassira et al, 1993) or locus coeruleus (Bouhassira et al, 1992a) did not modify DNIC in rodents. 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.…”

Section: Diffuse Noxious Inhibitory Controlmentioning

confidence: 99%

Stress-induced analgesia

Butler

Finn

2009

Progress in Neurobiology

558

420

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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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“…The physiological basis for CPM is supposed to lie mainly in the diffuse noxious inhibitory controls, which control the inhibition of nociceptive wide dynamic range neurons in the spinal and trigeminal horn elicited by noxious stimuli outside their receptive fields. The supraspinal components involved in CPM are assumed to be subnucleus reticularis dorsalis in the caudal medulla (Hu, 1990;Bouhassira et al, 1992), orbitofrontal cortex (Piché et al, 2009;Moont et al, 2011), amygdala (Piché et al, 2009;Moont et al, 2011), anterior cingulate cortex (Piché et al, 2009;Sprenger et al, 2011), primary somatosensory cortex (Piché et al, 2009) and the supplementary motor area (Piché et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Endogenous pain inhibition during menstrual cycle in migraine

Teepker

Kunz

Peters

et al. 2014

European Journal of Pain

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Background: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Methods: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Results: Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Conclusions: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.

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Involvement of the subnucleus reticularis dorsalis in diffuse noxious inhibitory controls in the rat

Cited by 176 publications

References 20 publications

Cerebral and Cerebrospinal Processes Underlying Counterirritation Analgesia

Cerebral and Cerebrospinal Processes Underlying Counterirritation Analgesia

Stress-induced analgesia

Endogenous pain inhibition during menstrual cycle in migraine

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