| 1. |
- Alhilou, AM, et al.
(författare)
-
Nerve growth factor and glutamate increase the density and expression of substance P-containing nerve fibers in healthy human masseter muscles
- 2021
-
Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1, s. 15673-
-
Tidskriftsartikel (refereegranskat)abstract
- Nocifensive behavior induced by injection of glutamate or nerve growth factor (NGF) into rats masseter muscle is mediated, in part, through the activation of peripheral NMDA receptors. However, information is lacking about the mechanism that contributes to pain and sensitization induced by these substances in humans. Immunohistochemical analysis of microbiopsies obtained from human masseter muscle was used to investigate if injection of glutamate into the NGF-sensitized masseter muscle alters the density or expression of the NMDA receptor subtype 2B (NR2B) or NGF by putative sensory afferent (that express SP) fibers. The relationship between expression and pain characteristics was also examined. NGF and glutamate administration increased the density and expression of NR2B and NGF by muscle putative sensory afferent fibers (P < 0.050). This increase in expression was greater in women than in men (P < 0.050). Expression of NR2B receptors by putative sensory afferent fibers was positively correlated with pain characteristics. Results suggest that increased expression of peripheral NMDA receptors partly contributes to the increased pain and sensitivity induced by intramuscular injection of NGF and glutamate in healthy humans; a model of myofascial temporomandibular disorder (TMD) pain. Whether a similar increase in peripheral NMDA expression occurs in patients with painful TMDs warrants further investigation.
|
|
| 2. |
- Alhilou, AM, et al.
(författare)
-
Sex-related differences in response to masseteric injections of glutamate and nerve growth factor in healthy human participants
- 2021
-
Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1, s. 13873-
-
Tidskriftsartikel (refereegranskat)abstract
- The neurophysiological mechanisms underlying NGF-induced masseter muscle sensitization and sex-related differences in its effect are not well understood in humans. Therefore, this longitudinal cohort study aimed to investigate the effect of NGF injection on the density and expression of substance P, NMDA-receptors and NGF by the nerve fibers in the human masseter muscle, to correlate expression with pain characteristics, and to determine any possible sex-related differences in these effects of NGF. The magnitude of NGF-induced mechanical sensitization and pain during oral function was significantly greater in women than in men (P < 0.050). Significant positive correlations were found between nerve fiber expression of NMDA-receptors and peak pain intensity (rs = 0.620, P = 0.048), and expression of NMDA-receptors by putative nociceptors and change in temporal summation pain after glutamate injection (rs = 0.561, P = 0.003). In women, there was a significant inverse relationship between the degree of NGF-induced mechanical sensitization and the change in nerve fiber expression of NMDA-receptors alone (rs = − 0.659, P = 0.013), and in combination with NGF (rs = − 0.764, P = 0.001). In conclusion, women displayed a greater magnitude of NGF-induced mechanical sensitization that also was associated with nerve fibers expression of NMDA-receptors, when compared to men. The present findings suggest that, in women, increased peripheral NMDA-receptor expression could be associated with masseter muscle pain sensitivity.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Bas, DB, et al.
(författare)
-
Pain in rheumatoid arthritis: models and mechanisms
- 2016
-
Ingår i: Pain management. - : Future Medicine Ltd. - 1758-1877 .- 1758-1869. ; 6:3, s. 265-84
-
Tidskriftsartikel (refereegranskat)abstract
- Pain is one of the most challenging symptoms for patients with rheumatoid arthritis (RA). RA-related pain is frequently considered to be solely a consequence of inflammation in the joints; however, recent studies show that multiple mechanisms are involved. Indeed, RA pain may start even before the disease manifests, and frequently does not correlate with the degree of inflammation or pharmacological management. In this aspect, animal studies have the potential to provide new insights into the pathology that initiate and maintain pain in RA. The focus of this review is to describe the most commonly used animal models for studies of RA pathology, which have also been utilized in pain research, and to summarize findings providing potential clues to the mechanisms involved in the regulation of RA-induced pain.
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
