The medullary dorsal reticular nucleus as a pronociceptive centre of the pain control system

Lima, Deolinda; Almeida, Armando

doi:10.1016/s0301-0082(01)00025-9

Cited by 125 publications

(119 citation statements)

References 253 publications

Supporting

Mentioning

110

Contrasting

Unclassified

Order By: Relevance

“…Pronociceptive actions are promoted by the PAG/ RVM circuit (Basbaum and Fields, 1984), classically involved in antinociception, depending on the intensity of the triggering stimulus (Lima and Almeida, 2002). Facilitation of the nociceptive response capacity mediated by RVM, a brainstem area receiving projections from PAG, is triggered by much less intense local chemical or electrical stimulation than that resulting on inhibition (Zhuo and Gebhart, 1997).…”

Section: Discussionmentioning

confidence: 99%

Signaling pathway of morphine induced acute thermal hyperalgesia in mice

Galeotti

Stefano

Guarna

et al. 2006

Pain

View full text Add to dashboard Cite

Systemic administration of morphine induced a hyperalgesic response in the hot plate test, at an extremely low dose (1-10 lg/kg). We have examined in vivo whether morphine, at an extremely low dose, induces acute central hypernociception following activation of the opioid receptor-mediated PLC/PKC inositol-lipid signaling pathway. The PLC inhibitor U73122 and the PKC blocker, calphostin C, dose dependently prevented the thermal hypernociception induced by morphine. This effect was also prevented by pretreatment with aODN against PLCb 3 at 2 nmol/mouse and PKCc at 2-3 nmol/mouse. Low dose morphine hyperalgesia was dose dependently reversed by selective NMDA antagonist MK801 and ketamine. This study demonstrates the presence of a nociceptive PLCb 3 /PKCc/NMDA pathway stimulated by low concentrations of morphine, through lOR 1 receptor, in mouse brain. This signaling pathway appears to play an opposing role in morphine analgesia. When mice were treated with a morphine analgesic dose (7 mg/kg), the downregulation of PLCb 3 or PKCc at the same aODN doses used for the prevention of the hyperalgesic effect induced, respectively, a 46% and 67% potentiation in analgesic response. Experimental and clinical studies suggest that opioid may activate pronociceptive systems, leading to pain hypersensitivity and short-term tolerance, a phenomenon encountered in postoperative pain management by acute opioid administration. The clinical management of pain by morphine may be revisited in light of the identification of the signaling molecules of the hyperalgesic pathway. Ó

show abstract

Section: Discussionmentioning

confidence: 99%

Signaling pathway of morphine induced acute thermal hyperalgesia in mice

Galeotti

Stefano

Guarna

et al. 2006

Pain

View full text Add to dashboard Cite

show abstract

“…However, other studies established that lesions of the RVM or the PAG did not block DNIC (130) and that DNIC was integrated at the level of the dorsal reticular nucleus (130). The dorsal reticular nucleus (DRt) receives nociceptive inputs from spinal projections and communicates with the PAG and RVM as well as the thalamus and amygdala and sends pain modulatory projections to the spinal cord (131)(132)(133). Moreover, the DRt sends and receives projections from cortical sites as well, and a single DRt neuron can project to different CNS sites, thus potentially modulating pain through several mechanisms (134).…”

Section: Diffuse Noxious Inhibitory Controls Modulation Of Painmentioning

confidence: 99%

Central modulation of pain

Ossipov¹,

Dussor²,

Porreca³

2010

J. Clin. Invest.

908

728

View full text Add to dashboard Cite

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.

show abstract

“…DNIC refers to the phenomenon whereby one noxious stimulus inhibits the pain produced by a second noxious stimulus (ie, counter-conditioning) [34]. In animal models, DNIC circuitry involves a spinobulbo-spinal negative feedback loop mediated by a supraspinal link in the medullary subnucleus reticularis dorsalis [35]. DNIC effects are demonstrated by assessing responses to a phasic noxious stimulus before and then during heterotopic application of a tonic noxious stimulus.…”

Section: Diffuse Noxious Inhibitory Controlsmentioning

confidence: 99%

Mechanisms by which sleep disturbance contributes to osteoarthritis pain: A conceptual model

Smith

Quartana²,

Okonkwo³

et al. 2009

Current Science Inc

126

View full text Add to dashboard Cite

Sleep disturbance is prevalent in aging and painful rheumatologic populations, but it has largely been a neglected dimension of the routine clinical care of arthritis patients. Pain associated with osteoarthritis (OA) is a leading cause of disability worldwide, and factors that contribute to pain in OA are poorly understood. Sleep disturbance is not only a consequence of pain, it is also likely to play an integral role in pain expression. Emerging research suggests that many patients with OA demonstrate signs of generalized hyperalgesia and faulty central pain modulatory processing similar to other idiopathic pain disorders, such as fibromyalgia. Sleep disruption is increasingly recognized as a direct contributor to both hyperalgesia and impaired endogenous pain modulation. This article reviews the extant literature on sleep disturbance and hyperalgesia in patients with OA. We propose a conceptual working model describing pathways by which sleep disturbance interacts directly with central pain processing mechanisms and inflammatory processes, and indirectly with mood and physical functioning to augment clinical OA pain. The clinical and research implications of the model are discussed.

show abstract

The medullary dorsal reticular nucleus as a pronociceptive centre of the pain control system

Cited by 125 publications

References 253 publications

Signaling pathway of morphine induced acute thermal hyperalgesia in mice

Signaling pathway of morphine induced acute thermal hyperalgesia in mice

Central modulation of pain

Mechanisms by which sleep disturbance contributes to osteoarthritis pain: A conceptual model

Contact Info

Product

Resources

About