Through our short-term observation, joint pain was effectively relieved and knee joint function was improved with systematic quadriceps isometric contraction exercise.

Chronic long-term exposure to cuprizone causes severe brain demyelination in mice, which leads to changes in locomotion, working memory and anxiety. These fi ndings suggest the importance of intact myelin for these behaviors. This study aimed to investigate the possible behavioral changes in mice with mild oligodendrocyte/myelin damage that parallels the white matter changes seen in the brains of patients with psychiatric disporders. We used the cuprizonetreated mouse model to test both tissue changes and behavioral functions (locomotor activity, anxiety status, and spatial working memory). The results showed that mice given cuprizone in their diet for 7 days had no significant myelin breakdown as evaluated by immunohistochemical staining for myelin basic protein, while the number of mature oligodendrocytes was reduced. The number and length of Caspr protein clusters, a structural marker of the node of Ranvier, did not change. The locomotor activity of the cuprizonetreated mice increased whereas their anxiety levels were lower than in normal controls; spatial working memory, however, did not change. These results, for the first time, link emotion-related behavior with mild white matter damage in cuprizone-treated mice.

Inflammatory pain is one of the most common types of chronic pain observed in the clinic and is usually caused by peripheral tissue inflammation and damage (Fan et al., 2014;Kidd & Urban, 2001).Nonsteroidal anti-inflammatory drugs are widely considered the first choice and effective drugs for the treatment of inflammatory pain. However, nonsteroidal anti-inflammatory drugs cause a wide range of alarming adverse effects, including gastrointestinal injury, cardiovascular events, and kidney failure (Bindu et al., 2020). Further investigation of the mechanism associated with inflammatory pain is crucial for developing new pharmacological treatments.

Chronic pain has detrimental effects on one’s quality of life. However, its treatment options are very limited, and its underlying pathogenesis remains unclear. Recent research has suggested that fragile X mental retardation protein is involved in the development of chronic pain, making it a potential target for prevention and treatment. The current review of literature will examine the function of fragile X mental retardation protein and its associated pathways, through which we hope to gain insight into how fragile X mental retardation protein may contribute to nociceptive sensitization and chronic pain.