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Journal of Diabetes Research
Volume 2014, Article ID 626108, 11 pages
Research Article

Decreased Neuronal Bursting and Phase Synchrony in the Hippocampus of Streptozotocin Diabetic Rats

1Key Laboratory of Brain Functional Genomics (MOE & STCSM), Institute of Cognitive Neuroscience, School of Psychology and Cognitive Science, East China Normal University, No. 3663 North Zhongshan Road, Shanghai 200062, China
2Department of Biomedical Engineering, School of Medicine, Tsinghua University, No. 16 Shuangqing Road, Beijing 100084, China
3School of Biomedical Engineering, Fourth Military Medical University, No. 169 Changle West Road, Xi’an 710032, China
4Department of Anesthesiology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai 200032, China

Received 31 March 2014; Accepted 19 May 2014; Published 29 June 2014

Academic Editor: Konstantinos Papatheodorou

Copyright © 2014 Zhimei Qiao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetic encephalopathy is one of the complications of diabetes. Cognitive dysfunction is the main consequence. Previous findings from neuroanatomical and in vitro electrophysiological studies showed that the structure and function of the hippocampus is impaired in diabetes, which may underlie the cognitive dysfunction induced by diabetes. However the study of electrophysiological abnormality of hippocampal neurons in intact networks is sparse. In the current study, we recorded the spontaneous firing of neurons in hippocampal CA1 area in anesthetized streptozotozin (STZ)-diabetic and age-matched control rats. Profound reduction in burst activity was found in diabetic rats. Compared to control rats, the intra-burst inter-spike intervals were prolonged significantly in diabetic rats, while the burst ratio and the mean number of spikes within a burst decreased significantly. Treatment with APP 17-mer peptide retarded the effects of diabetes on these parameters. In addition, the average PLV of diabetic rats was lower than that of control rats. These findings provide in vivo electrophysiological evidence for the impairment of hippocampal function in STZ-diabetic rats, and may have some implications in the mechanisms associated with cognitive deficits in diabetes.