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Science:可自由开关实验鼠脑神经回路新技术

来源:Science 2008-01-28 09:45

生物谷报道:美国麻省理工学院教授、诺贝尔奖得主利根川进在24日的美国《科学》杂志网络版上报告说,他们开发出一种可自由开关实验鼠脑神经回路的技术。

利根川进是日本唯一一名诺贝尔生理学或医学奖得主,现为美国麻省理工学院脑科学中心负责人。他领导的研究小组通过转基因技术将控制破伤风毒素合成的基因植入实验鼠,并使基因只在实验鼠某些特定的神经细胞中发挥作用。

破伤风毒素生效后,神经细胞就不能释放出信号,神经回路被切断。如果在实验鼠的饲料中添加盐酸多西环素,抑制毒素活动,神经回路又会得以恢复。如果再喂食不含盐酸多西环素的普通饲料,实验鼠神经回路会再次被断开。

在实验中,研究人员利用这种技术自由开闭实验鼠大脑海马部位的三突触回路。利根川进认为,这一成果将成为探究大脑记忆和学习能力的重要研究手段。(生物谷援引新华网)

生物谷推荐原始出处:

Published Online January 24, 2008
Science DOI: 10.1126/science.1151120

Submitted on September 28, 2007
Accepted on January 11, 2008

Transgenic Inhibition of Synaptic Transmission Reveals Role of CA3 Output in Hippocampal Learning

Toshiaki Nakashiba 1, Jennie Z. Young 1, Thomas J. McHugh 1, Derek L. Buhl 1, Susumu Tonegawa 1*

1 The Picower Institute for Learning and Memory, Howard Hughes Medical Institute, RIKEN-MIT Neuroscience Research Center, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

* To whom correspondence should be addressed.
Susumu Tonegawa , E-mail: tonegawa@mit.edu

The hippocampus is an area of the brain involved in learning and memory. It contains parallel excitatory pathways referred to as the trisynaptic pathway (which carries information from the entorhinal cortex -> dentate gyrus -> CA3 -> CA1 -> entorhinal cortex) and the monosynaptic pathway (which connects entorhinal cortex -> CA1 -> entorhinal cortex). We developed a generally applicable tetanus toxin-based method for transgenic mice that permits inducible and reversible inhibition of synaptic transmission and applied it to the trisynaptic pathway while preserving transmission in the monosynaptic pathway. We found that synaptic output from CA3 in the trisynaptic pathway is dispensable and the short monosynaptic pathway is sufficient for incremental spatial learning. In contrast, the full trisynaptic pathway containing CA3 is required for rapid, one-trial contextual learning, for pattern completionbased memory recall and for spatial tuning of CA1 cells.

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