SIGMA-1 Receptor Gene Variants Affect the Somatosensory Phenotype in Neuropathic Pain Patients.


Journal

The journal of pain
ISSN: 1528-8447
Titre abrégé: J Pain
Pays: United States
ID NLM: 100898657

Informations de publication

Date de publication:
02 2019
Historique:
received: 17 10 2017
revised: 16 08 2018
accepted: 28 08 2018
pubmed: 30 9 2018
medline: 8 9 2020
entrez: 30 9 2018
Statut: ppublish

Résumé

Pain sensitivity is characterized by interindividual variability, determined by factors including genetic variation of nociceptive receptors and pathways. The sigma-1 receptor (SIGMAR1) is involved in pain modulation especially under pre-sensitized conditions. However, the contribution of SIGMAR1 genetic variants to pain generation and sensitivity is unknown yet. This study aimed to identify effects of 5 SIGMAR1 variants on the somatosensory phenotype of neuropathic pain patients (n = 228) characterized by standardized quantitative sensory testing. Principal component analysis revealed that the SIGMAR1 variants -297G>T (rs10814130) and 5A>C (rs1800866) significantly lowered thermal detection and heat/pressure nociception in particular in neuropathic pain patients with mainly preserved somatosensory function. Compared to wild-type, the variant allele -297T was associated with loss of warm detection (P = .049), lower heat-pain sensitivity (P = .027) and wind-up ratio (P = .023) as well as increased paradoxical heat sensation (P = .020). Likewise for 5A>C the strongest genotype-associated differences observed were reduced peripheral (less heat hyperalgesia; P = .026) and central sensitization (lower mechanical pain sensitivity; P = .026) in variant compared to wild-type carriers. This study indicates lack of association of SIGMAR1 -297G>T and 5A>C genetic variants to susceptibility to develop chronic pain, but significant modulation of somatosensory function in neuropathic pain patients. PERSPECTIVE: This article presents the first study indicating a modulation of somatosensory function in neuropathic pain patients by selected genetic variants in SIGMAR1. As our findings could contribute to the explanation of interindividual differences in drug response they might help to improve the treatment of neuropathic pain.

Identifiants

pubmed: 30266269
pii: S1526-5900(18)30618-7
doi: 10.1016/j.jpain.2018.08.011
pii:
doi:

Substances chimiques

Receptors, sigma 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

201-214

Informations de copyright

Copyright © 2018 the American Pain Society. Published by Elsevier Inc. All rights reserved.

Auteurs

Juliane Sachau (J)

Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany; Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Henrike Bruckmueller (H)

Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Janne Gierthmühlen (J)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Walter Magerl (W)

Center of Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Meike Kaehler (M)

Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Sierk Haenisch (S)

Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Andreas Binder (A)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Amke Caliebe (A)

Institute of Medical Informatics and Statistics, Kiel University, Kiel, Germany.

Christoph Maier (C)

Department of Pain Management, BG Universitätsklinikum Bergmannsheil, Ruhr-University Bochum, Bochum, Germany.

Rolf-Detlef Treede (RD)

Center of Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Thomas Tölle (T)

Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.

Ingolf Cascorbi (I)

Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. Electronic address: cascorbi@pharmakologie.uni-kiel.de.

Ralf Baron (R)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

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Classifications MeSH