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Regulation of Spontaneous Neural Activity by Channel-Mediated Co...

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  • 2014-01-22

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BK21 Program of Bio-Molecular Function Seminar



 



▶Subject : Regulation of Spontaneous Neural Activity by Channel-Mediated Copper Signaling



 



▶Speaker : Christine I. Nam (University of California)



 



▶Date :PM 2:00/May 27(THU.)/2010



 



▶Place :Rm 104, Life Science Bldg



 



*Abstract


The brain requires the highest levels of metal nutrients in the body for normal function, including copper and related transition metals at concentrations an order of magnitude greater than found in other tissues. In this context, copper is traditionally viewed as a static cofactor for metalloenzymes, but its interactions with known proteins cannot fully account for the need for elevated copper levels in the brain. Here we report the discovery that copper plays a dynamic and essential role in regulating basal neural activity. Treatment of primary neuronal cultures with copper-specific chelators triggers marked increases in uncontrolled synchronous activity as determined by whole-field calcium imaging. Likewise, neurons from mice lacking the copper-specific channel Ctr1 also show elevated spikes in synchronous activity compared to wild-type neurons, with disruption of homeostatic copper levels shown by copper-selective fluorescent indicators. Furthermore, diminished copper uptake through Ctr1 results in a loss of inhibitory GABA compensation that correlates with hyper spontaneous responses, and copper rescue can restore normal activity patterns. Our findings provide establish a fundamental role for copper in neural function and support an emerging paradigm of copper as a dynamic metal signal in living systems



 



☎ Inquiry: Prof. Kyong Tai Kim(279-2297)



 




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