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The Journal of Neuroscience, April 8, 2009, 29(14):4681-4685; doi:10.1523/JNEUROSCI.0297-09.2009

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Brief Communications
Presynaptic Defects Underlying Impaired Learning and Memory Function in Lipoprotein Lipase-Deficient Mice

Xunde Xian,^1 * Tingting Liu,^2 * Jia Yu,^2 * Yuhui Wang,¹ Yifei Miao,² Jianjun Zhang,³ Yan Yu,² Colin Ross,⁴ Joanna M. Karasinska,⁴ Michael R. Hayden,⁴ George Liu,¹ and Dehua Chui²

¹Institute of Cardiovascular Sciences and Key Laboratory of Molecular Cardiovascular Sciences and ²Neuroscience Research Institute and Department of Neurobiology, Key Laboratory for Neuroscience, Ministry of Education, Key Laboratory for Neuroscience, Ministry of Public Health, Health Science Center, Peking University, Beijing 100191, China, ³Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing 100050, China, and ⁴Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada V5T 4H4

Correspondence should be addressed to either Dr. George Liu or Dr. Dehua Chui, Peking University Health Science Center, 38 Xueyuan Road, Hai Dian District, Beijing 100191, China, Email: vangeorgeliu{at}gmail.com or Email: dchui{at}bjmu.edu.cn

Lipoprotein lipase (LPL) is predominantly expressed in adipose and muscle where it plays a crucial role in the metabolism of triglyceride-rich plasma lipoproteins. LPL is also expressed in the brain with highest levels found in the pyramidal cells of the hippocampus, suggesting a possible role for LPL in the regulation of cognitive function. However, very little is currently known about the specific role of LPL in the brain. We have generated a mouse model of LPL deficiency which was rescued from neonatal lethality by somatic gene transfer. These mice show no exogenous and endogenous LPL expression in the brain. To study the role of LPL in learning and memory, the performance of LPL-deficient mice was tested in two cognitive tests. In a water maze test, LPL-deficient mice exhibited increased latency to escape platform and increased mistake frequency. Decreased latency to platform in the step-down inhibitory avoidance test was observed, consistent with impaired learning and memory in these mice. Transmission electron microscopy revealed a significant decrease in the number of presynaptic vesicles in the hippocampus of LPL-deficient mice. The levels of the presynaptic marker synaptophysin were also reduced in the hippocampus, whereas postsynaptic marker postsynaptic density protein 95 levels remained unchanged in LPL-deficient mice. Theses findings indicate that LPL plays an important role in learning and memory function possibly by influencing presynaptic function.

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Received Jan. 18, 2009; accepted March 1, 2009.

Correspondence should be addressed to either Dr. George Liu or Dr. Dehua Chui, Peking University Health Science Center, 38 Xueyuan Road, Hai Dian District, Beijing 100191, China, Email: vangeorgeliu{at}gmail.com or Email: dchui{at}bjmu.edu.cn

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