N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats

IMR OpenIR

	N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats
其他题名	N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats
	Zhu Qiwen; Hou Weijian; Zhao Jianwen; Yang Yu; Zhang Qi; Guo Li; Shang Lihong; Cao Yinglin; Wu Chunfu
	2010
发表期刊	NEURAL REGENERATION RESEARCH
ISSN	1673-5374
卷号	5 期号:23 页码:1787-1794
摘要	Lead exposure induces decreased hippocampal N-methyl-D-aspartic acid (NMDA) receptor gene and protein expressions, which influences the molecular mechanisms of learning and memory. However, lead poisoning-induced differences in NMDA subunit expression, and the correlation of lead poisoning with learning and memory, remain poorly understood. The present study measured differences in expression of NMDA receptor subunits NR1, NR2A, and NR2B in memory-related brain regions of rats who underwent different doses of lead exposure. Results demonstrated decreased NR1, NR2A, and NR2B subunit expressions in some memory-related brain areas. The inhibitory effect of 4.8 mmol/L lead exposure on hippocampal NR2B was most significant, although NR2A expression also significantly decreased following 14.4 mmol/L lead exposure. There was no difference in NR1 expression following exposure to <4.8 mmol/L lead, although the inhibitory effect of 19.6 mmol/L lead exposure was strongest for NR1 expression in the hippocampus. Inhibitory avoidance test results revealed that greater concentrations of lead exposure resulted in decreased learning and memory. Therefore, lead toxicity was dependent on NMDA receptor subunit composition, and NR1, NR2A, and NR2B expressions were associated with time and concentration of lead exposure.
其他摘要	Lead exposure induces decreased hippocampal N-methyl-D-aspartic acid (NMDA) receptor gene and protein expressions, which influences the molecular mechanisms of learning and memory. However, lead poisoning-induced differences in NMDA subunit expression, and the correlation of lead poisoning with learning and memory, remain poorly understood. The present study measured differences in expression of NMDA receptor subunits NR1, NR2A, and NR2B in memory-related brain regions of rats who underwent different doses of lead exposure. Results demonstrated decreased NR1, NR2A, and NR2B subunit expressions in some memory-related brain areas. The inhibitory effect of 4.8 mmol/L lead exposure on hippocampal NR2B was most significant, although NR2A expression also significantly decreased following 14.4 mmol/L lead exposure. There was no difference in NR1 expression following exposure to < 4.8 mmol/L lead, although the inhibitory effect of 19.6 mmol/L lead exposure was strongest for NR1 expression in the hippocampus. Inhibitory avoidance test results revealed that greater concentrations of lead exposure resulted in decreased learning and memory. Therefore, lead toxicity was dependent on NMDA receptor subunit composition, and NR1, NR2A, and NR2B expressions were associated with time and concentration of lead exposure
关键词	SURFACE EXPRESSION MESSENGER-RNA HIPPOCAMPAL NEUROTOXICITY DISEASE SYSTEM INJURY WATER lead exposure N-methyl-D-aspartate receptor memory-related brain areas neural regeneration rats
收录类别	CSCD
语种	英语
资助项目	[Science and Technology Bureau of Liaoning Province]
CSCD记录号	CSCD:4100499
引用统计
文献类型	期刊论文
条目标识符	http://ir.imr.ac.cn/handle/321006/144129
专题	中国科学院金属研究所
作者单位	中国科学院金属研究所
推荐引用方式 GB/T 7714	Zhu Qiwen,Hou Weijian,Zhao Jianwen,et al. N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats[J]. NEURAL REGENERATION RESEARCH,2010,5(23):1787-1794.
APA	Zhu Qiwen.,Hou Weijian.,Zhao Jianwen.,Yang Yu.,Zhang Qi.,...&Wu Chunfu.(2010).N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats.NEURAL REGENERATION RESEARCH,5(23),1787-1794.
MLA	Zhu Qiwen,et al."N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats".NEURAL REGENERATION RESEARCH 5.23(2010):1787-1794.