The effect of modification of 5-hydroxytryptamine function in nucleus raphe magnus on nociceptive threshold

Llewelyn, Meirion B.; Azami, J.; Roberts, M. W.

doi:10.1016/0006-8993(84)90365-2

Cited by 38 publications

(11 citation statements)

References 31 publications

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“…Consistent with this hypothesis, classical pharmacological studies in uninjured animals show microinjection of 5-HT or a SERT inhibitor into the RVM increases the tail flick latency, blockade of serotonin receptors in the RVM prevents analgesia produced by stimulation of the PAG, systemic morphine increases 5-HT in the RVM, and application of 5-HT to RVM neurons excites 66% of RVM cells[33, 37, 38, 60]. Thus, we propose that increases in serotonin in the RVM mediate analgesia while decreases in serotonin mediate hyperalgesia.…”

Section: Discussionmentioning

confidence: 86%

Short-duration physical activity prevents the development of activity-induced hyperalgesia through opioid and serotoninergic mechanisms

Lima

DeSantana

Rasmussen

et al. 2017

Pain

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Regular physical activity prevents the development of chronic muscle pain through the modulation of central mechanisms that involve rostral ventromedial medulla (RVM). We tested if pharmacological blockade or genetic deletion of mu-opioid receptors in physically active mice modulates excitatory and inhibitory systems in the RVM in an activity-induced hyperalgesia model. We examined response frequency to mechanical stimulation of the paw, muscle withdrawal thresholds, and expression of phosphorylation of the NR1 subunit of the N-methyl-D-aspartate receptor (p-NR1) and serotonin transporter (SERT) in the RVM. Mice that had performed 5 days of voluntary wheel running prior to the induction of the model were compared with sedentary mice. Sedentary mice showed significant increases in mechanical paw withdrawal frequency and a reduction in muscle withdrawal threshold; wheel running prevented the increase in paw withdrawal frequency. Naloxone-treated and MOR−/− mice had increases in withdrawal frequency that were significantly greater than that in physically active control mice and similar to sedentary mice. Immunohistochemistry in the RVM showed increases in p-NR1 and SERT expression in sedentary mice 24 hours after the induction of the model. Wheel running prevented the increase in SERT, but not p-NR1. Physically active, naloxone-treated, and MOR−/− mice showed significant increases in SERT immunoreactivity when compared with wild-type physically active control mice. Blockade of SERT in the RVM in sedentary mice reversed the activity-induced hyperalgesia of the paw and muscle. These results suggest that analgesia induced by 5 days of wheel running is mediated by mu-opioid receptors through the modulation of SERT, but not p-NR1, in RVM.

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Section: Discussionmentioning

confidence: 86%

Short-duration physical activity prevents the development of activity-induced hyperalgesia through opioid and serotoninergic mechanisms

Lima

DeSantana

Rasmussen

et al. 2017

Pain

View full text Add to dashboard Cite

show abstract

“…Despite evidence for 5-HT controls within the RVMM (Llewelyn et al, 1983(Llewelyn et al, , 1984Wessendorf and Anderson, 1983;Willcockson et al ., 1983 ;Inase, 1987;585 Pan et al ., 1993 ) and evidence for serotonergic terminals that contact serotonergic somata or proximal dendrites (Potrebic et al ., 1995), little is known about the source of the 5-HT released in this region . The RVMM is rich in 5-HT-immunoreactive terminals (Steinbush, 1981 ;Chazal and Ma, 1989) .…”

Section: Origin Of Medullary Dialysate 5-htmentioning

confidence: 95%

Neurochemical Characterization of Extracellular Serotonin in the Rostral Ventromedial Medulla and Its Modulation by Noxious Stimuli

Taylor

Basbaum

1995

Journal of Neurochemistry

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Using in vivo microdialysis, we have characterized serotonin release from the rostral ventromedial medulla of the freely moving rat. Addition of tetrodotoxin or removal of calcium from the dialysis solution diminished the dialysate serotonin content, suggesting that spontaneous, calcium channel‐ and sodium channel‐dependent neuronal release mechanisms contribute to the extracellular serotonin collected from the rostral ventromedial medulla. Extracellular serotonin concentration was increased by depolarization (with 100 mM potassium) and by the local administration of either a reuptake blocker (citalopram), a monoamine oxidase inhibitor (pargyline), or amphetamine. Serotonin release was reduced significantly by 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin, suggesting that serotonin1A receptors may regulate release from rostral ventromedial medulla neurons. Because the basal serotonin concentration in the rostral ventromedial medulla was approximately twofold higher than that collected from the rostral ventrolateral medulla, a region that contains serotonin terminals but many fewer cell bodies, the possibility of release of serotonin from rostral ventromedial medulla neurons is discussed. Finally, intraplantar formalin injection significantly increased serotonin release, suggesting that this neurotransmitter contributes to nociceptive modulation by regulating the outflow of the rostral ventromedial medulla neurons.

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“…The fact that all anti-depressants may not be effective indicates that the therapeutic effect is probably not due to a general mood improvement (99, 100) but may be dependent on the individual monoamine uptake inhibition profile or other as yet unknown properties of the anti-depressant in question. Furthermore, amine uptake inhibitors are known to elevate nociceptive thresholds (13,101,102).…”

Section: Migraine and Depressive Disordersmentioning

confidence: 99%

The Platelet and The Neuron: Two Cells in Focus in Migraine

Malmgren

Hasselmark

1988

Cephalalgia

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Reports of platelet abnormalities in migraine are abundant, and the present paper discusses the role of platelets in the migraine aetiology. Platelets are considered good models for pre- and post-synaptic functions in serotonergic neurons. We propose that migraine is associated with a lowered threshold for stimulus response in both platelets and serotonergic neurons and that the alterations in platelet function reflect central serotonergic disturbances. The platelet abnormalities in migraine approach those found in depression, and there are several links between the two disorders. The clinical significance of platelet hyperactivity in migraineurs for the occurrence of thrombotic disorders is also discussed. Studies of platelet functions in migraine, using platelets as models for serotonergic neurons, may broaden our understanding of the neuronal processes that take place during a migraine attack. The platelet can also be an investigative tool for better understanding of the modes of action of anti-migraine drugs.

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The effect of modification of 5-hydroxytryptamine function in nucleus raphe magnus on nociceptive threshold

Cited by 38 publications

References 31 publications

Short-duration physical activity prevents the development of activity-induced hyperalgesia through opioid and serotoninergic mechanisms

Short-duration physical activity prevents the development of activity-induced hyperalgesia through opioid and serotoninergic mechanisms

Neurochemical Characterization of Extracellular Serotonin in the Rostral Ventromedial Medulla and Its Modulation by Noxious Stimuli

The Platelet and The Neuron: Two Cells in Focus in Migraine

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