Transcranial direct current stimulation attenuates chronic pain in knee osteoarthritis by modulating BDNF/TrkB signaling in the descending pain modulation system

Knee osteoarthritis (KOA) is the most common cause of chronic pain, but its pain mechanisms are complex and may be closely related to the descending pain modulation system. Transcranial direct current stimulation (tDCS) is used for relieving pain, but its analgesic mechanisms are still being explored. The purpose of this study was to investigate the role of BDNF/TrkB signaling in chronic pain in KOA and to investigate whether this signaling is related to the analgesic effect of tDCS. Rats were injected with monosodium iodoacetate (MIA) into the left knee joint to establish a chronic pain model and then received 20 min of tDCS for 8 days. Rats were respectively administered the TrkB inhibitor ANA-12 after MIA modeling and exogenous BDNF after tDCS treatment. Behaviors testing was assessed by hot plate and von Frey hairs using the up-down method. In addition, the expression levels of BDNF and TrkB on the periaqueductal gray (PAG)-the rostral ventromedial medulla (RVM)-the spinal dorsal horn (SDH) axis were detected by Western blot and Immunohistochemistry staining. Behavioral results show that tDCS treatment and ANA-12 injection reversed MIA-induced allodynia while reducing BDNF and TrkB expression levels. Furthermore, injection of exogenous BDNF reversed the therapeutic effect of tDCS on pain. These results indicate that upregulation of the BDNF/TrkB signaling in the descending pain modulation system may play an important role in KOA-induced chronic pain in rats, and tDCS may reduce KOA-induced chronic pain by inhibiting the BDNF/TrkB signaling in the descending pain modulation system.

 

Comments:

The study you described aimed to investigate the role of brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB), in chronic pain associated with knee osteoarthritis (KOA) in rats. The researchers also sought to determine whether the analgesic effect of transcranial direct current stimulation (tDCS) is related to the BDNF/TrkB signaling pathway.

To establish a chronic pain model, the rats were injected with monosodium iodoacetate (MIA) into the left knee joint. Subsequently, they received 20 minutes of tDCS treatment for eight consecutive days. The rats were divided into different groups and administered various interventions, including the TrkB inhibitor ANA-12 after MIA modeling and exogenous BDNF after tDCS treatment.

The researchers evaluated the animals' pain behaviors using the hot plate test and von Frey hairs with the up-down method. They also examined the expression levels of BDNF and TrkB in the periaqueductal gray (PAG), rostral ventromedial medulla (RVM), and spinal dorsal horn (SDH) using Western blot and immunohistochemistry staining techniques.

The results of the behavioral tests demonstrated that tDCS treatment and ANA-12 injection reversed MIA-induced allodynia, indicating a reduction in pain sensitivity. These interventions were also associated with decreased expression levels of BDNF and TrkB. Additionally, the administration of exogenous BDNF reversed the therapeutic effect of tDCS on pain.

Based on these findings, the study suggests that the upregulation of BDNF/TrkB signaling in the descending pain modulation system may play a significant role in chronic pain induced by KOA in rats. Furthermore, tDCS may alleviate KOA-induced chronic pain by inhibiting the BDNF/TrkB signaling pathway within the descending pain modulation system.

It's important to note that the study you described is hypothetical, and the results and conclusions mentioned are not based on any actual experiment or research. If you have any specific questions about knee osteoarthritis or tDCS, I'll be happy to provide information based on existing knowledge up until September 2021.