Introduction: Pain is a complex experience that involves various components, including sensory, cognitive, and emotional. Augmented response to pain is one of the short-term complications of diabetes. This complication can be caused by a disturbance in the transmission and processing of pain signals. Diabetes can be associated with neuro-physiological and structural changes in the brain. Insulin roles in the central nervous system have been less studied. This study aimed to investigate the pain pathway in the central nervous system in the absence of peripheral insulin. Methodsand Materials: Sixty adult male rats were studied in six groups. Diabetes was induced by Streptozotocin (STZ) (60 mg/kg, IP). Insulin (5 mU/animal, 5 μL) was injected into the left ventricle of groups 2, 3, and 6. The pain was induced by subcutaneous injection of 50 μL of 2.5% formalin in the right hind paw. Samples were collected at 4 weeks after diabetes induction. Glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), and receptors of advanced glycation end products (RAGE) were measured using the RT-qPCR. Results: In the indicated nuclei of diabetic rats, the expression levels of NSE and RAGE genes were increased, while the expression level of GFAP showed a decrease. These results confirm the results observed in the formalin test regarding the analgesic effect of insulin in non-diabetic rats. Conclusion: We conclude that ICV injection of insulin reduces the sensation of pain, but this effect is not observed due to cell damage in the thalamus, raphe magnus, and PAG because of diabetes in those rats. Also, insulin improves the pathological effects of diabetes in the brain.
Basatinya A M, Sajedianfard J, Hosseinzadeh S. Lack of peripheral insulin and intraventricular injection of insulin and its effect on pain sensation pathway in short-term diabetes. Koomesh 2023; 25 (5) :78-78 URL: http://koomeshjournal.semums.ac.ir/article-1-8187-en.html