title: What do monoamines do in pain modulation?
abstract: Here, we give a topical overview of the ways in which brain processing can alter spinal pain transmission through descending control pathways, and how these change in pain states. We link preclinical findings on the transmitter systems involved and discuss how the monoamines, noradrenaline, 5-hydroxytryptamine (5-HT), and dopamine, can interact through inhibitory and excitatory pathways.
  
  
  
  Descending pathways control sensory events and the actions of the neurotransmitters noradrenaline and 5-HT in the dorsal horn of the spinal cord are chiefly implicated in nociception or antinociception according to the receptor that is activated. Abnormalities in descending controls effect central pain processing. Following nerve injury a noradrenaline-mediated control of spinal excitability is lost, whereas its restoration reduces neuropathic hypersensitivity. The story with 5-HT remains more complex because of the myriad of receptors that it can act upon; however the most recent findings support that facilitations may dominate over inhibitions.
  
  
  
  The monoaminergic system can be manipulated to great effect in the clinic resulting in improved treatment outcomes and is the basis for the actions of the antidepressant drugs in pain. Looking to the future, prediction of treatment responses will possible by monitoring a form of inhibitory descending control for optimized pain relief.
authors.affiliation: Department Neuroscience, Physiology and Pharmacology, University College London, London, UK.
authors.forename: Kirsty
authors.initials: K
authors.lastname: Bannister
authors.forename: Anthony H
authors.initials: AH
authors.lastname: Dickenson
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists / Q000378:metabolism; D000700:Analgesics / Q000494:pharmacology* / Q000627:therapeutic use*; D000701:Analgesics, Opioid / Q000493:pharmacokinetics / Q000627:therapeutic use; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D000927:Anticonvulsants / Q000494:pharmacology / Q000627:therapeutic use; D000928:Antidepressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D015306:Biogenic Monoamines / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D009437:Neuralgia / Q000188:drug therapy / Q000503:physiopathology; D009638:Norepinephrine / Q000378:metabolism; D010146:Pain / Q000503:physiopathology*; D058748:Pain Perception / Q000502:physiology; D012701:Serotonin / Q000378:metabolism; D058827:Serotonin 5-HT3 Receptor Agonists / Q000378:metabolism; D013116:Spinal Cord / Q000378:metabolism*
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D000700:Analgesics; D000701:Analgesics, Opioid; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000927:Anticonvulsants; D000928:Antidepressive Agents; D015306:Biogenic Monoamines; D058827:Serotonin 5-HT3 Receptor Agonists; D012701:Serotonin; D004298:Dopamine; D009638:Norepinephrine