Effects of Streptozotocin-Induced Type 1 Diabetes on Cell Proliferation and Neuronal Differentiation in the Dentate Gyrus; Correlation with Memory Impairment.
- Author:
Jung Hoon CHOI
1
;
In Koo HWANG
;
Sun Shin YI
;
Ki Yeon YOO
;
Choong Hyun LEE
;
Hyung Cheul SHIN
;
Yeo Sung YOON
;
Moo Ho WON
Author Information
1. Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chuncheon 200-702, Korea. mhwon@hallym.ac.kr
- Publication Type:Original Article
- Keywords:
Streptozotocin;
Type 1 diabetes;
Passive avoidance test;
Ki67;
Doublecortin
- MeSH:
Cell Proliferation;
Dendrites;
Dentate Gyrus;
Humans;
Male;
Memory;
Neurons;
Rats, Wistar;
Retention (Psychology);
Streptozocin
- From:Korean Journal of Anatomy
2009;42(1):41-48
- CountryRepublic of Korea
- Language:English
-
Abstract:
We examined the effects of steptozotocin (STZ)-induced type 1 diabetes on cell proliferation and neuroblasts in the subgranular zone of the hippocampal dentate gyrus (SZDG) of male Wistar rats. Change in memory function was also investigated using the passive avoidance test. In the SZDG, Ki67 (a marker for cell proliferation) positive nuclei were significantly decreased at 2 and 3 weeks and slightly decreased at 4 weeks after STZ treatment. Doublecortin (DCX, a marker for neuronal differentiation)-immunoreactive (+) neuroblasts with tertiary dendrites were significantly decreased in the STZ-treated group compared to those in the vehicle-treated group. However, DCX+ neuroblasts without tertiary dendrites were abundant at 4 weeks after STZ treatment. In addition, retention latency time in STZ-treated group was similar to that of vehicle-treated group at 2 and 3 weeks after STZ treatment. However, the retention latency time was significantly decreased at 4 weeks after STZ treatment. These results suggest that STZ significantly reduced cell proliferation and neuroblasts at 2~3 weeks after STZ treatment, but not at 4 weeks after STZ treatment although memory impairment was detected at 4 weeks after STZ treatment. The gradual reduction of DCX+ neuroblasts with tertiary dendrites may be associated with the impairment of hippocampus-related memory function.
