Kamei Junzo, Zushida Ko, Miyata Shigeo
Department of Pathophysiology and Therapeutics, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41, Ebara, Shinagawa-ku, Tokyo, 142-8501 Japan.
Nihon Shinkei Seishin Yakurigaku Zasshi. 2002 Aug;22(4):121-9.
Diabetic neuropathy is a most-convoluted complication. Diabetic gastropathy, ulcers, diarrhea, and bladder dysfunction are the major peripheral neuropathies. Peripheral neuropathies have been the primary neuroscience focus of diabetes research. In contrast to the periphery, the brain is not usually thought to be a target of chronic diabetic complications. However, the impact of diabetes mellitus on the central nervous system has recently gained attention. It is well known that diabetes or hyperglycemia influences the sensitivity of laboratory animals to various pharmacological agents. An increased sensitivity of hyperglycemic or diabetic animals to barbiturates and a decreased sensitivity of D-amphetamine, p-chloroamphetamine, and carbon tetrachloride have been demonstrated. Furthermore, it was reported that mice and rats with streptozotocin-induced diabetes and spontaneously diabetic mice are significantly less sensitive than non-diabetic mice to the antinociceptive effect of morphine. However, little information is available regarding the mechanism responsible for these changes. It is well established that anxiety and depression are common in patients with diabetes. Moreover, diabetic animals showed significantly more anxiogenic activity than non-diabetic animals did. However, the mechanisms through which diabetes may contribute to the development of, or be a risk factor for, psychiatric disorders are not clear. We provide an overview of our current understanding of the effects of streptozotocin-induced diabetes on the opioid receptor and the benzodiazepine receptor.
