Unilateral injection of Aβ25–35 in the hippocampus reduces the number of dendritic spines in hyperglycemic rats. Issue 12 (13th August 2014)

• Record Type: Journal Article
• Authors: Lazcano, Zayda; Solis, Oscar; Bringas, María Elena; Limón, Daniel; Diaz, Alfonso; Espinosa, Blanca; García‐Peláez, Isabel; Flores, Gonzalo; Guevara, Jorge
• Is Part Of: Synapse. Volume 68:Issue 12(2014:Dec.)
• Page Start: 585
• Page End: 594
• Publication Date: 2014-08-13
• Subjects: Synapses -- Periodicals; 612
• DOI: 10.1002/syn.21770
• Languages: English
• ISSNs: 0887-4476

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>Alzheimer'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 Aβ_25–35 unilateral injection into the Hp. Our results demonstrate that STZ combined with Aβ_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 Aβ_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 Aβ‐induced neurodegeneration and thus the appearance of AD symptoms would be accelerated. <bold>Synapse 68:585–594, 2014</bold>. © 2014 Wiley Periodicals, Inc.</p> </abstract>