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Central Modulation of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Serotonin is a major neurotransmitter in descending pathways. There is a high level of serotonin in nucleus raphe magnus cells and in terminals of descending fibres in the dorsal horn. Electrical stimulation of the nucleus raphe magnus increases the release of serotonin in the spinal cord.
Pain
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
There are three major components of the endogenous analgesic pathway: Periaqueductal gray areaNucleus raphe magnusPain inhibitory complex in the dorsal horns of the spinal cord
Anatomy and Physiology of Pain: The Central and Peripheral Nervous Systems
Published in Gary W. Jay, Chronic Pain, 2007
Stimulation-produced analgesia (SPA) in the nucleus raphe magnus or local CNS opioid injections can activate the MAS. The interaction with the opioid system occurs both supraspinally and in the dorsal horn of the spinal cord. SPA, as the words indicate, occurs when a specific part of the CNS is electrically stimulated.
HYPNOTIZABILITY-RELATED FAAH C385A POLYMORPHISM: POSSIBLE ENDOCANNABINOID CONTRIBUTION TO SUGGESTION-INDUCED ANALGESIA
Published in International Journal of Clinical and Experimental Hypnosis, 2020
Silvano Presciuttini, Giancarlo Carli, Enrica L. Santarcangelo
Interestingly, the effects of small differences in the FAAH activity could be amplified by the interactions of eCB with other neurotransmitters, beyond opiates that are scarcely effective in highs (Presciuttini et al., 2018). A mechanism responsible for hypnotizability-related differences in suggestion-induced analgesia could consist of greater response of noradrenegic and dopaminergic neurons to eCBs. In fact, noradrenergic and eCBs pathways converge onto several brain regions – the nucleus accumbens, the locus coeruleus, the nucleus of solitary tract, and the medial prefrontal cortex – and the modulation of the activity of eCBs receptors CB1 alters the indices of nor-adrenergic activity (Scavone, Sterling, & Van Bockstaele, 2013). Moreover, in the basal ganglia circuits eCBs interact with dopaminergic pathways (Di Filippo et al., 2008). Another candidate to account for suggestion-induced analgesia is the oxytocin (OXT) released in the brain and possibly modulating the sensory and emotional components of pain (Poisbeau, Grinevich, & Charlet, 2018). OXT axons innervate the periaqueductal gray matter, nucleus raphe magnus, nucleus accumbens, central amygdala, and cortical areas. Central injection of OXT reduces pain through the endogenous opioid system but also by regulating the eCBs production (Russo et al., 2012). Different variants of the OXT gene have been associated with slightly different hypnotizability levels – one point out of 12 on standard scales (Bryant, Hung, Dobson-Stone, & Schofield, 2013) – although the direct comparison between highs, lows and controls has not revealed significant differences (Presciuttini et al., 2018).
Persistent effects of the orexin-1 receptor antagonist SB-334867 on naloxone precipitated morphine withdrawal symptoms and nociceptive behaviors in morphine dependent rats
Published in International Journal of Neuroscience, 2021
Masoumeh Kourosh-Arami, Mohammad-Taghi Joghataei, Alireza Komaki, Masoumeh Gholami, Zohreh Najafi, Mostafa Lavaie
Long-term administration of OXR1 antagonist, SB-334867, prior to morphine injection, significantly increased morphine tolerance at inter- or late-phase of the formalin-induced pain in this study. Most orexin neurons express morphine receptors and produce c-Fos in response to morphine. Additionally, some studies have revealed that intra-periaqueductal gray administration (a supraspinal site) of orexin-A may produce antinociceptive effects [31]. Other studies have reported that SB-334867 inhibits morphine- [30,42] and stress-induced antinociception [43]. Based on the evidence above, it seems that orexin may demonstrate an intrinsic antinociceptive effect by itself. Therefore, the antinociceptive effect of morphine in the formalin-induced pain might be due to regulation of orexinergic cells or modulation of descending inhibitory pathways by orexin-A [30,42]. Thus, orexin can reduce pain similar to morphine. Furthermore, some elements related to antinociception are mediated by the orexinergic system through the activation of OXR1. Moreover, acute injection of SB-334867 combined with morphine did not produce hyperalgesia. Therefore, put together, our finding may suggest that long-term injection of SB-334867 along with morphine during neural development might have a synergistic effect on morphine tolerance, and hence lead to hyperalgesia. Nucleus raphe magnus, which is a thermoregulatory center, possesses high densities of not only opiate receptors but also orexin receptors [12,44,45]. Raphe magnus serotonergic neurons tonically modify nociceptive transmission [46]. Therefore, it may be postulated that SB-334867 may induce hyperalgesia by changing the modulatory effect of raphe magnus on nociception. Nucleus tractus solitarius as a center of cardiovascular regulation also is involved in hyperalgesia [47,48]. Hence, SB-induced hyperalgesia may result from activation of this nucleus.