Insulin Within the Arcuate Nucleus Has Paradoxical Effects on Nociception in Healthy and Diabetic Rats

• Published in: Basic and clinical neuroscience Vol. 11; no. 6; pp. 727 - 736
• Main Authors: Khaleghzadeh-Ahangar, Hossein, Sadeghimahalli, Forouzan, Khandan, Shaghayegh, Shahabi, Sima, Moghadamnia, Aliakbar
• Format: Journal Article
• Language: English
• Published: Tehran Negah Scientific Publisher 01-11-2020; Iranian Neuroscience Society; Iran University of Medical Sciences
• Subjects: acute pain; Arcuate nucleus; Diabetes; Diabetes mellitus (insulin dependent); hot plate; Hypothalamus; Insulin; Insulin receptors; Latency; Lidocaine; Neural networks; Pain perception; Proopiomelanocortin; Research Paper; Streptozocin; tail-flick; the arcuate nucleus
• ISSN: 2228-7442; 2008-126X; 2228-7442
• DOI: 10.32598/bcn.11.6.1983.1

Introduction: Broad neural circuits originate from the hypothalamic arcuate nucleus and project to many parts of the brain which are related to pain perception. Insulin receptors are found in the arcuate nucleus. Since nociception may be affected in type 1 diabetes, the present study aimed to investigate the intra-arcuate nucleus insulin role in pain perception in streptozotocin (STZ)-induced diabetic and healthy rats. Methods: Regular insulin was microinjected within the arcuate nucleus and the pain tolerance was measured using the hot plate and the tail-flick apparatus in diabetic rats. Results: The results showed that the arcuate nucleus suppression with lidocaine could increase thermal nociception in non-diabetic animals. Also, insulin within the arcuate nucleus decreased the acute thermal pain perception in these animals. STZ-induced diabetes produced hypoalgesia which the latency of these tests, progressively increased over time after induction of diabetes. Also, in the same animal group, intra-arcuate injection of insulin reduced the latency of nociception. Conclusion: Intra-arcuate insulin has paradoxical and controversial effects in healthy and diabetic rats’ nociception. These effects seem to be due to the insulin effect on releasing pro-opiomelanocortin and its deriv