Streptozotocin-induced insulin deficiency leads to development of behavioral deficits in rats

Diabetes mellitus is one of the most common serious metabolic disorders in humans that develops due to diminished production of insulin (type I) or resistance to its effect (type II and gestational). The present study was designed to determine the neuropsychological deficits produced following streptozotocin-induced diabetes in rats. Rats were made diabetic by the intra-peritoneal administration of 60 mg/kg streptozotocin (STZ) which induces type-1 diabetes by the destruction “β-cells” of pancreas. Body weight, food and water intake was monitored daily. Open field test (OFT) model, forced swim test (FST) and Morris water maze (MWM) model were performed for the evaluation of ambulation, depression-like symptoms and memory effects, respectively. After 10 days of diabetes induction the exploratory activity of rats was monitored by OFT while depression-like symptoms and memory effects in rats were analyzed by FST and MWM. Results showed that there was no significant effect of STZ-induced diabetes on body weight but food and water intake of STZ-induced diabetic rats was significantly increased. Exploratory activity was significantly decreased and short-term and long-term memory was significantly impaired while the depression-like symptoms was significantly increased in STZ diabetic rats. Thus, it may be suggested that STZ-induced diabetes alters the brain functions and may play an important role in the pathophysiology of certain behavioral deficits like depression, impaired learning and memory functions related to diabetes. This finding may be of relevance in the pathophysiology and in the clinical picture, which could be related to an altered brain serotonin metabolism and neurotransmission and may possibly be related to neuropsychiatric disorders in diabetic patients.