Serotonin and nociception: from nociceptive transduction at the periphery to pain modulation from the brain

Martins, Daniel Oliveira

doi:10.1016/b978-0-12-813323-1.00012-8

Cited by 2 publications

(1 citation statement)

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“…First of all, serotonin (5-HT) plays an important role in nociceptive processing; among others, via descending inhibitory serotonergic projections from the nucleus raphe magnus to the spinal cord (Basbaum & Fields 1984;Feng et al 2012). As animal studies have shown, these descending serotonergic projections can both inhibit as well as facilitate nociception, depending on the site of action and on the receptor subtype (Martins 2019). Given this complexity of action, it is not surprising that the role of 5-HT in experimental and clinical pain could still not be finally clarified in human studies, although there is some indication that low central levels of 5-HT might be associated with increased clinical pain complaints (Goesling et al 2013;Cooper et al 2017, Nagata et al 2007.…”

Section: Introductionmentioning

confidence: 99%

Facial expressions of pain: the role of the serotonergic system

Kunz,

Bär,

Karmann

et al. 2023

Psychopharmacology

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Rationale Although interest in the neurobiology of facial communication of pain has increased over the last decades, little is known about which neurotransmitter systems might be involved in regulating facial expressions of pain. Objectives We aim to investigate whether the serotonergic system (5-HT), which has been implicated in various aspects of pain processing as well as in behavioral response inhibition, might play a role in facial expressions of pain. Using acute tryptophan depletion (ATD) to manipulate 5-HT function, we examined its effects on facial and subjective pain responses. Methods In a double-blind, placebo-controlled within-subject design, 27 participants received either an ATD or a control drink in two separate sessions. Approximately 5-h post-oral consumption, we assessed pain thresholds (heat, pressure) as well as facial and subjective responses to phasic heat pain. Moreover, situational pain catastrophizing and mood were assessed as affective state indicators. Results ATD neither influenced pain thresholds nor self-report ratings, nor catastrophizing or mood. Only facial responses were significantly affected by ATD. ATD led to a decrease in pain-indicative as well as in pain-non-indicative facial responses to painful heat, compared to the control condition. Conclusions Decrease in brain 5-HT synthesis via ATD significantly reduced facial responses to phasic heat pain; possibly due to (i) diminished disposition to display social behavior or due to (ii) decreased facilitation of excitatory inputs to the facial motor neuron.

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