Insulin Treatment Prevents the Increase in D-Serine in Hippocampal CA1 Area of Diabetic Rats. (March 2015)

• Record Type: Journal Article
• Authors: Yang, Jing; Song, Yang; Wang, Hongxin; Liu, Chunna; Li, Zhongzhe; Liu, Ying; Kong, Yawei
• Is Part Of: American journal of Alzheimer's disease & other dementias. Volume 30:Number 2(2015)
• Page Start: 201
• Page End: 208
• Publication Date: 2015-03
• Subjects: insulin -- d-serine -- long-term potentiation -- water maze -- serine racemase; Alzheimer's disease -- Periodicals; Dementia -- Periodicals; Alzheimer's disease -- Patients -- Care -- United States -- Periodicals; 616.83
• DOI: 10.1177/1533317514545379
• Languages: English
• ISSNs: 1533-3175

Abstract

Purpose: Diabetes is a high risk factor for dementia. Employing a diabetic rat model, the present study was designed to determine whether the content ofd -serine (d -Ser) in hippocampus is associated with the impairment of spatial learning and memory ability. Methods: Diabetes was induced by a single intravenous injection of streptozotocin (STZ). The insulin treatment began 3 days after STZ injection. Results: We found that both water maze learning and hippocampal CA1 long-term potentiation (LTP) were impaired in diabetic rats. The contents of glutamate, d -Ser, and serine racemase in the hippocampus of diabetic rats were significantly higher than those in the control group. Insulin treatment prevented the STZ-induced impairment in water maze learning and hippocampal CA1-LTP in diabetic rats and also maintained the contents of glutamate, d -Ser, and serine racemase at the normal range in hippocampus. Conclusions: These results suggest that insulin treatment has a potent protection effect on CA1-LTP, spatial learning and memory ability of the diabetic rats in vivo . Furthermore, insulin may take effect by inhibiting the overactivation of N -methyl-d -aspartate receptors, which play a critical role in neurotoxicity.