Serotonergic neuromodulation of peripheral nociceptors

Abstract

Nociception, the encoding and processing of noxious environmental stimuli by sensory neurons, functions to protect an organism from bodily damage. Activation of the terminal endings of certain sensory neurons, termed nociceptors, triggers a train of impulses to neurons in the spinal cord. Signals are integrated and processed in the dorsal spinal cord and then projected to the brain where they elicit the perception of pain. A number of neuromodulators that can affect nociceptors are released in the periphery during the inflammation that follows an initial injury. Serotonin (5-HT) is a one such proinflammatory mediator. This review discusses our current understanding of the neuromodulatory role of 5-HT, and specifically how this monoamine activates and sensitizes nociceptors. Potential therapeutic targets to treat pain are described.

Serotonergic modulation of pain and analgesic responses: A study in rats with constitutionally altered serotonin transporters

“…Serotonin has complex modulatory roles in the physiological control of pain messages: in the periphery, it reinforces pain, whereas in the central nervous system, it exerts primarily inhibitory, but also excitatory, effects on the nociception (Bardin, 2011;Loyd et al, 2013;Viguier et al, 2013). Serotonin has complex modulatory roles in the physiological control of pain messages: in the periphery, it reinforces pain, whereas in the central nervous system, it exerts primarily inhibitory, but also excitatory, effects on the nociception (Bardin, 2011;Loyd et al, 2013;Viguier et al, 2013).…”

“…It is known that 5HT released from platelets following initial cell injury activates nociceptors and exerts proalgesic effects acting directly or through facilitation of other peripheral pain mediators (Sommer, 2010;Loyd et al, 2013). It is known that 5HT released from platelets following initial cell injury activates nociceptors and exerts proalgesic effects acting directly or through facilitation of other peripheral pain mediators (Sommer, 2010;Loyd et al, 2013).…”

“…The role of serotonin (5-hydroxytryptamine, 5HT) systems in modulating nociception has long been recognized, and increased activity of brain serotonergic neurons is associated with analgesia and enhanced antinociceptive drug potency (Sommer, 2010;Loyd et al, 2013). Recently, it has become clear that 5HT, acting centrally and/or peripherally, exerts both algesic and analgesic effects, depending upon the site of action, nature of nociceptive stimuli and subtypes of activated 5HT receptors (Bardin, 2011;Viguier et al, 2013).…”

Balanophora spicataand Lupeol Acetate Possess Antinociceptive and Anti-Inflammatory ActivitiesIn VivoandIn Vitro

“…The effect of BS crude extract on carrageenan-induced paw edema is similar to indomethacin. Owing to serotonin is a proinflammatory mediator [20], the anti-inflammatory effect of BS crude extract on serotonin-induced edema was further assessed. The BS crude extract at higher dose (250 mg/kg) notably inhibited the serotonin-induced edema.…”

Peripheral and spinal mechanisms of nociception in a rat reserpine-induced pain model

“…27 Potential consequences of peripheral monoamine depletion are unknown, although neuromodulatory effects of these transmitters on nociceptors are well described. 12,23,24 Under hyperalgesic conditions, such as inflammation and neuropathy, many ion channels that are responsible for pain, mechanotransduction, and generation/propagation of action Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. potentials are upregulated in DRG neurons.…”