GLP-2 restores impairments in spatial working memory and hippocampal LTD via the MEK/ERK pathway in juvenile-onset diabetes rats

被引：8
作者：
Sasaki-Hamada, Sachie [1 ,2 ]
Fujiwara, Ayumu [1 ]
Satoh, Show [1 ]
Iwai, Takashi [3 ]
Oka, Jun-Ichiro [1 ]
机构：
[1] Tokyo Univ Sci, Fac Pharmaceut Sci, Lab Pharmacol, 2641 Yamazaki, Noda, Chiba 2788510, Japan
[2] Kitasato Univ, Sch Allied Hlth Sci, Dept Physiol, Sagamihara, Kanagawa 2520373, Japan
[3] Kitasato Univ, Sch Pharmaceut Sci, Lab Pharmacol, Tokyo 1088641, Japan
来源：
BEHAVIOURAL BRAIN RESEARCH | 2021年 / 406卷
关键词：
Diabetes; Streptozotocin; Learning; Synaptic plasticity; Hippocampus; GLP-2; GLUCAGON-LIKE PEPTIDE-2; LONG-TERM DEPRESSION; SYNAPTIC PLASTICITY; IMPROVEMENT; ACTIVATION; EXPRESSION; RECEPTOR; NMDA; MICE;
D O I：
10.1016/j.bbr.2021.113235
中图分类号：
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号：
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要：
Type 1 diabetic animal models, generated by injecting streptozotocin (STZ), have been widely used in research. We previously reported that juvenile-onset diabetes mellitus (JDM) rats, which were prepared by administering STZ to 17-day-old rats, developed cognitive impairments and hippocampal synaptic plasticity deficiencies, which were restored by glucagon-like peptide-1 (GLP-1). GLP-1 and GLP-2 are simultaneously derived from proglucagon and act through their own specific receptors. The present study was performed to investigate the potential of GLP-2 in JDM rats. The results obtained demonstrated that GLP-2 restored impairments in spatial working memory and hippocampal long-term depression (LTD) in JDM rats, and that the MEK1/2 inhibitor, U0126, inhibited this recovery. Therefore, GLP-2 has potential in the treatment of cognitive deficits in childhood-onset diabetes.
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页数：5
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