An evaluation of the genetic conditioning of evoking pain.

Abstract

Pain is an integral element of the pathogenic process and sometimes determines its course. Disorders in pain sensation, as well as its lack, the pain threshold, and variability in sensation of the same pain stimuli as more or less intensive by different persons, may be genetically conditioned. The aim of the study is to examine genes in pathogenesis of chronic pain. The study was conducted in a specially selected group of 31 persons: study group - 20 patients with chronic pain, and control group - 11 healthy individuals who did not experience pain. The control group of 11 healthy persons, compared with the study group, was the catalyst for determining the relative quantification (RQ) of gene expression. Biological material in the form of venous blood was collected from the study participants into the tubes containing anticoagulant EDTA KE/2.7 ml (ethylenediaminetetraacetic acid), preventing extracorporeal blood clotting. Analysis of expression of the examined genes showed over-expression of the DRD1 gene in patients experiencing chronic pain, which means that in these patients an increased number of dopamine D1 receptors encoded by this gene should be expected. The dopamine D1 receptor is a G-protein-coupled receptor which regulates (stimulates or inhibits) adenyl cyclase - the enzyme responsible for synthesis of cyclic AMP (cAMP). An increase in the concentration of cAMP in neurons enhances the sensation of pain. The genes (DRD1, COMT, OPRK1, HCN2) have a significant role in the pathogenesis of chronic pain in various diseases; they can also influence the perception of pain. Knowledge of these genes can contribute to the development of effective methods of combating pain.