Abstract:
:Threohydroxyaspartate (THA)-induced glutamate excitotoxicity in organotypic culture of rat spinal cord is a well-known model of motor neuron degeneration. THA causes accumulation of synaptic glutamate and over stimulation of the postsynaptic receptor by inhibiting glutamate uptake. This model has also been used to identify agents that inhibit glutamate excitotoxicity by increasing the expression of glutamate transporter. We now show that THA also increases iron level in rat spinal cord tissue, with concomitant modulation of key iron transport and storage proteins, including transferrin receptor, divalent metal-ion transporter 1 and ferritin. More significantly, iron chelator deferoxamine (DFO) was able to completely prevent THA-induced motor neuron degeneration. The protective effect of DFO did not involve enhancing glutamate uptake. These data provide new mechanistic insight into THA-induced glutamate excitotoxicity and suggest that blocking THA-induced iron rise alone may be sufficient for prevention of glutamate excitotoxicity.
journal_name
Brain Resjournal_title
Brain researchauthors
Yu J,Guo Y,Sun M,Li B,Zhang Y,Li Cdoi
10.1016/j.brainres.2008.12.030subject
Has Abstractpub_date
2009-02-27 00:00:00pages
102-7eissn
0006-8993issn
1872-6240pii
S0006-8993(08)03006-0journal_volume
1257pub_type
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