Skip to main content
Top
Published in: Journal of Neurology 2/2018

Open Access 01-02-2018 | Review

Advances in understanding nociception and neuropathic pain

Author: Ewan St. John Smith

Published in: Journal of Neurology | Issue 2/2018

Login to get access

Abstract

Pain results from the activation of a subset of sensory neurones termed nociceptors and has evolved as a “detect and protect” mechanism. However, lesion or disease in the sensory system can result in neuropathic pain, which serves no protective function. Understanding how the sensory nervous system works and what changes occur in neuropathic pain are vital in identifying new therapeutic targets and developing novel analgesics. In recent years, technologies such as optogenetics and RNA-sequencing have been developed, which alongside the more traditional use of animal neuropathic pain models and insights from genetic variations in humans have enabled significant advances to be made in the mechanistic understanding of neuropathic pain.
Literature
4.
go back to reference Crook RJ, Walters ET (2011) Nociceptive behavior and physiology of molluscs: animal welfare implications. ILAR J 52:185–195CrossRefPubMed Crook RJ, Walters ET (2011) Nociceptive behavior and physiology of molluscs: animal welfare implications. ILAR J 52:185–195CrossRefPubMed
10.
go back to reference Lewin GR, Lechner SG, Smith ESJ (2014) Nerve growth factor and nociception: from experimental embryology to new analgesic therapy. Handb Exp Pharmacol 220:251–282CrossRefPubMed Lewin GR, Lechner SG, Smith ESJ (2014) Nerve growth factor and nociception: from experimental embryology to new analgesic therapy. Handb Exp Pharmacol 220:251–282CrossRefPubMed
14.
go back to reference Calabrò A, Caterino AL, Elefante E et al (2016) One year in review 2016: novelties in the treatment of rheumatoid arthritis. Clin Exp Rheumatol 34:357–372PubMed Calabrò A, Caterino AL, Elefante E et al (2016) One year in review 2016: novelties in the treatment of rheumatoid arthritis. Clin Exp Rheumatol 34:357–372PubMed
18.
go back to reference Breivik H, Collett B, Ventafridda V et al (2006) Survey of chronic pain in Europe: prevalence, impact on daily life, and treatment. Eur J Pain 10:287–333CrossRefPubMed Breivik H, Collett B, Ventafridda V et al (2006) Survey of chronic pain in Europe: prevalence, impact on daily life, and treatment. Eur J Pain 10:287–333CrossRefPubMed
19.
go back to reference Riskowski JL (2014) Associations of socioeconomic position and pain prevalence in the United States: findings from the National Health and Nutrition Examination Survey. Pain Med 15:1508–1521. doi:10.1111/pme.12528 CrossRefPubMed Riskowski JL (2014) Associations of socioeconomic position and pain prevalence in the United States: findings from the National Health and Nutrition Examination Survey. Pain Med 15:1508–1521. doi:10.​1111/​pme.​12528 CrossRefPubMed
26.
28.
go back to reference Hockley JRF, González-Cano R, McMurray S et al (2017) Visceral and somatic pain modalities reveal NaV 1.7-independent visceral nociceptive pathways. J Physiol 595:2661–2679. doi:10.1113/JP272837 CrossRefPubMed Hockley JRF, González-Cano R, McMurray S et al (2017) Visceral and somatic pain modalities reveal NaV 1.7-independent visceral nociceptive pathways. J Physiol 595:2661–2679. doi:10.​1113/​JP272837 CrossRefPubMed
31.
go back to reference Immke DC, McCleskey EW (2001) Lactate enhances the acid-sensing Na+ channel on ischemia-sensing neurons. Nat Neurosci 4:869–870CrossRefPubMed Immke DC, McCleskey EW (2001) Lactate enhances the acid-sensing Na+ channel on ischemia-sensing neurons. Nat Neurosci 4:869–870CrossRefPubMed
38.
go back to reference Weir GA, Middleton SJ, Clark AJ et al (2017) Using an engineered glutamate-gated chloride channel to silence sensory neurons and treat neuropathic pain at the source. Brain. doi:10.1093/brain/awx201 PubMed Weir GA, Middleton SJ, Clark AJ et al (2017) Using an engineered glutamate-gated chloride channel to silence sensory neurons and treat neuropathic pain at the source. Brain. doi:10.​1093/​brain/​awx201 PubMed
43.
go back to reference Burma NE, Leduc-Pessah H, Fan CY, Trang T (2017) Animal models of chronic pain: advances and challenges for clinical translation: animal models of chronic pain. J Neurosci Res 95:1242–1256. doi:10.1002/jnr.23768 CrossRefPubMed Burma NE, Leduc-Pessah H, Fan CY, Trang T (2017) Animal models of chronic pain: advances and challenges for clinical translation: animal models of chronic pain. J Neurosci Res 95:1242–1256. doi:10.​1002/​jnr.​23768 CrossRefPubMed
45.
go back to reference Hama A, Takamatsu H (2016) Chemotherapy-induced peripheral neuropathic pain and rodent models. CNS Neurol Disord Drug Targets 15:7–19CrossRefPubMed Hama A, Takamatsu H (2016) Chemotherapy-induced peripheral neuropathic pain and rodent models. CNS Neurol Disord Drug Targets 15:7–19CrossRefPubMed
50.
go back to reference Gracely RH, Lynch SA, Bennett GJ (1992) Painful neuropathy: altered central processing maintained dynamically by peripheral input. Pain 51:175–194CrossRefPubMed Gracely RH, Lynch SA, Bennett GJ (1992) Painful neuropathy: altered central processing maintained dynamically by peripheral input. Pain 51:175–194CrossRefPubMed
57.
go back to reference Zakrzewska JM, Palmer J, Morisset V et al (2017) Safety and efficacy of a Nav1.7 selective sodium channel blocker in patients with trigeminal neuralgia: a double-blind, placebo-controlled, randomised withdrawal phase 2a trial. Lancet Neurol 16:291–300. doi:10.1016/S1474-4422(17)30005-4 CrossRefPubMed Zakrzewska JM, Palmer J, Morisset V et al (2017) Safety and efficacy of a Nav1.7 selective sodium channel blocker in patients with trigeminal neuralgia: a double-blind, placebo-controlled, randomised withdrawal phase 2a trial. Lancet Neurol 16:291–300. doi:10.​1016/​S1474-4422(17)30005-4 CrossRefPubMed
59.
64.
go back to reference Priest BT, Murphy BA, Lindia JA et al (2005) Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior. Proc Natl Acad Sci USA 102:9382–9387CrossRefPubMedPubMedCentral Priest BT, Murphy BA, Lindia JA et al (2005) Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior. Proc Natl Acad Sci USA 102:9382–9387CrossRefPubMedPubMedCentral
69.
go back to reference Blackburn-Munro G, Jensen BS (2003) The anticonvulsant retigabine attenuates nociceptive behaviours in rat models of persistent and neuropathic pain. Eur J Pharmacol 460:109–116CrossRefPubMed Blackburn-Munro G, Jensen BS (2003) The anticonvulsant retigabine attenuates nociceptive behaviours in rat models of persistent and neuropathic pain. Eur J Pharmacol 460:109–116CrossRefPubMed
71.
go back to reference Momin A, Cadiou H, Mason A, McNaughton PA (2008) Role of the hyperpolarization-activated current Ih in somatosensory neurons. J Physiol 586:5911–5929CrossRefPubMedPubMedCentral Momin A, Cadiou H, Mason A, McNaughton PA (2008) Role of the hyperpolarization-activated current Ih in somatosensory neurons. J Physiol 586:5911–5929CrossRefPubMedPubMedCentral
80.
go back to reference Wetzel C, Hu J, Riethmacher D et al (2007) A stomatin-domain protein essential for touch sensation in the mouse. Nature 445:206–209CrossRefPubMed Wetzel C, Hu J, Riethmacher D et al (2007) A stomatin-domain protein essential for touch sensation in the mouse. Nature 445:206–209CrossRefPubMed
81.
go back to reference Wetzel C, Pifferi S, Picci C et al (2016) Small-molecule inhibition of STOML3 oligomerization reverses pathological mechanical hypersensitivity. Nat Neurosci 20:209–218. doi:10.1038/nn.4454 CrossRefPubMed Wetzel C, Pifferi S, Picci C et al (2016) Small-molecule inhibition of STOML3 oligomerization reverses pathological mechanical hypersensitivity. Nat Neurosci 20:209–218. doi:10.​1038/​nn.​4454 CrossRefPubMed
84.
go back to reference Eaton MJ, Plunkett JA, Karmally S et al (1998) Changes in GAD- and GABA-immunoreactivity in the spinal dorsal horn after peripheral nerve injury and promotion of recovery by lumbar transplant of immortalized serotonergic precursors. J Chem Neuroanat 16:57–72CrossRefPubMed Eaton MJ, Plunkett JA, Karmally S et al (1998) Changes in GAD- and GABA-immunoreactivity in the spinal dorsal horn after peripheral nerve injury and promotion of recovery by lumbar transplant of immortalized serotonergic precursors. J Chem Neuroanat 16:57–72CrossRefPubMed
86.
go back to reference Polgár E, Hughes DI, Riddell JS et al (2003) Selective loss of spinal GABAergic or glycinergic neurons is not necessary for development of thermal hyperalgesia in the chronic constriction injury model of neuropathic pain. Pain 104:229–239CrossRefPubMed Polgár E, Hughes DI, Riddell JS et al (2003) Selective loss of spinal GABAergic or glycinergic neurons is not necessary for development of thermal hyperalgesia in the chronic constriction injury model of neuropathic pain. Pain 104:229–239CrossRefPubMed
93.
Metadata
Title
Advances in understanding nociception and neuropathic pain
Author
Ewan St. John Smith
Publication date
01-02-2018
Publisher
Springer Berlin Heidelberg
Published in
Journal of Neurology / Issue 2/2018
Print ISSN: 0340-5354
Electronic ISSN: 1432-1459
DOI
https://doi.org/10.1007/s00415-017-8641-6

Other articles of this Issue 2/2018

Journal of Neurology 2/2018 Go to the issue