期刊
NATURE NEUROSCIENCE
卷 5, 期 2, 页码 155-161出版社
NATURE AMERICA INC
DOI: 10.1038/nn791
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资金
- NIMH NIH HHS [MH48147] Funding Source: Medline
- NINDS NIH HHS [NS28462, NS42156] Funding Source: Medline
Induction and expression of long-term potentiation (LTP) in area CA1 of the hippocampus require the coordinated regulation of several cellular processes. We found that LTP in area CA1 was associated with an N-methyl-D-aspartate (NMDA) receptor-dependent increase in glutamate uptake. The increase in glutamate uptake was inhibited by either removal of Na+ or addition of D, L-threo-beta-hydroxyaspartate. Dihydrokainate (DHK), a specific inhibitor of the glial glutamate transporter GLT-1, did not block the increase in glutamate uptake. LTP was also associated with a translocation of the EAAC1 glutamate transporter from the cytosol to the plasma membrane. Contextual fear conditioning increased the maximum rate (V-max) of glutamate uptake and membrane expression of EAAC1 in area CA1. These results indicate that regulation of glutamate uptake may be important for maintaining the level of synaptic strength during long-term changes in synaptic efficacy.
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