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Unilateral injection of Aβ 25–35 in the hippocampus reduces the number of dendritic spines in hyperglycemic rats
Author(s) -
Lazcano Zayda,
Solis Oscar,
Bringas María Elena,
Limón Daniel,
Diaz Alfonso,
Espinosa Blanca,
GarcíaPeláez Isabel,
Flores Gonzalo,
Guevara Jorge
Publication year - 2014
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.21770
Subject(s) - dendritic spine , hippocampus , morris water navigation task , neurodegeneration , streptozotocin , neuroscience , synapse , neurochemical , hippocampal formation , medicine , endocrinology , biology , diabetes mellitus , disease
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. Synapse 68:585–594, 2014 . © 2014 Wiley Periodicals, Inc.