Unilateral Injection of A beta(25-35) in the Hippocampus Reduces the Number of Dendritic Spines in Hyperglycemic Rats

作者：Lazcano Zayda; Solis Oscar; Elena Bringas Maria; Limon Daniel; Diaz Alfonso; Espinosa Blanca; Garcia Pelaez Isabel; Flores Gonzalo; Guevara Jorge^*

来源：Synapse, 2014, 68(12): 585-594.

DOI：10.1002/syn.21770

• Alzheimer
• animal models
• hyperglycemia
• spatial memory
• dendritic spine
• dorsal hippocampus

Alzheimer%26apos;s disease (AD) is a neurodegenerative process exacerbated by several risk factors including impaired glucose metabolism in the brain that could cause molecular and neurochemical alterations in cognitive regions such as the hippocampus (Hp). Consequently, this process could cause neuronal morphological changes; however, the mechanism remains elusive. We induced chronic hyperglycemia after streptozotocin (STZ) administration. Then, we examined spatial learning and memory using the Morris water maze test and evaluated neuronal morphological changes using the Golgi-Cox stain procedure in hyperglycemic rats that received a A(25-35) unilateral injection into the Hp. Our results demonstrate that STZ combined with A(25-35) induced significant deficits in the spatial memory. In addition, we observed a significant reduction in the number of dendritic spines of pyramidal neurons in the dorsal Hp of rats with STZ plus A(25-35). In conclusion, the reduced spine density of pyramidal neurons in the CA1 dorsal Hp could produce the spatial memory deficit observed in these animals. These results suggest that hyperglycemia can trigger A-induced neurodegeneration and thus the appearance of AD symptoms would be accelerated. Synapse 68:585-594, 2014.

• 出版日期2014-12