| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Research Abstract |
There is evidence that diabetes condition is associated with hippocampal impairment, although how this occurs is not clear. In this study we investigated pathological roles of ERK, an important component in the regulation of synaptic plasticity, in diabetes-induced spine dysmorphogenesis. The inhibition of ERK activity was observed in streptozotocin-induced diabetic mice and high glucose-treated neuron. Chronic high-glucose treatment impaired insulin signaling in vitro models of diabetes. Administration of 17beta-estradiol (E2) and its derivative (E2A) leaded to activation of ERK both in vivo and in vitro. These results suggest that Insulin receptor dysfunction may play a role in chronic hyperglycemia-induced hippocampal impairment, and that E2 is a promising therapeutic drug for diabetic spine dysmorphogenesis.
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