Neuropathic Pain Dysregulates Gene Expression of the Forebrain Opioid and Dopamine Systems.
Animals
Corpus Striatum
/ metabolism
Enkephalins
/ biosynthesis
Gene Expression
Male
Mice
Neuralgia
/ genetics
Pain Measurement
/ methods
Prosencephalon
/ metabolism
Protein Precursors
/ biosynthesis
Receptors, Dopamine
/ biosynthesis
Receptors, Opioid, delta
/ biosynthesis
Receptors, Opioid, kappa
/ biosynthesis
Receptors, Opioid, mu
/ biosynthesis
Chronic pain
Dopamine
Mesostriatal system
Neuropathy
Nucleus accumbens
Opioids
Journal
Neurotoxicity research
ISSN: 1476-3524
Titre abrégé: Neurotox Res
Pays: United States
ID NLM: 100929017
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
received:
30
04
2019
accepted:
22
01
2020
revised:
17
01
2020
pubmed:
7
2
2020
medline:
22
12
2020
entrez:
7
2
2020
Statut:
ppublish
Résumé
Disturbances in the function of the mesostriatal dopamine system may contribute to the development and maintenance of chronic pain, including its sensory and emotional/cognitive aspects. In the present study, we assessed the influence of chronic constriction injury (CCI) of the sciatic nerve on the expression of genes coding for dopamine and opioid receptors as well as opioid propeptides in the mouse mesostriatal system, particularly in the nucleus accumbens. We demonstrated bilateral increases in mRNA levels of the dopamine D1 and D2 receptors (the latter accompanied by elevated protein level), opioid propeptides proenkephalin and prodynorphin, as well as delta and kappa (but not mu) opioid receptors in the nucleus accumbens at 7 to 14 days after CCI. These results show that CCI-induced neuropathic pain is accompanied by a major transcriptional dysregulation of molecules involved in dopaminergic and opioidergic signaling in the striatum/nucleus accumbens. Possible functional consequences of these changes include opposite effects of upregulated enkephalin/delta opioid receptor signaling vs. dynorphin/kappa opioid receptor signaling, with the former most likely having an analgesic effect and the latter exacerbating pain and contributing to pain-related negative emotional states.
Identifiants
pubmed: 32026358
doi: 10.1007/s12640-020-00166-4
pii: 10.1007/s12640-020-00166-4
pmc: PMC7085470
doi:
Substances chimiques
Enkephalins
0
Protein Precursors
0
Receptors, Dopamine
0
Receptors, Opioid, delta
0
Receptors, Opioid, kappa
0
Receptors, Opioid, mu
0
proenkephalin
0
preproenkephalin
93443-35-7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
800-814Subventions
Organisme : National Science Centre, Poland
ID : MAESTRO 2012/06/NZ4/00028
Organisme : National Science Centre, Poland
ID : OPUS 2018/29/B/NZ7/00082
Organisme : European Commission
ID : #HEALTH-F2-2013-602891
Organisme : Ministry of Science and Higher Education, Poland
ID : KNOW scholarship
Organisme : Ministry of Science and Higher Education, Poland
ID : KNOW scholarship
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