| First Author | Huang S | Year | 2018 |
| Journal | Brain Res | Volume | 1678 |
| Pages | 129-137 | PubMed ID | 29066369 |
| Mgi Jnum | J:268236 | Mgi Id | MGI:6271129 |
| Doi | 10.1016/j.brainres.2017.10.011 | Citation | Huang S, et al. (2018) Astrocytic glutamatergic transporters are involved in Abeta-induced synaptic dysfunction. Brain Res 1678:129-137 |
| abstractText | In Alzheimer's disease (AD), dementia severity correlates most strongly with decreased synapse density in the hippocampus and cerebral cortex. Although studies in rodents have established that hippocampal long-term potentiation (LTP) is inhibited by soluble oligomers of beta-amyloid (Abeta), the synaptic mechanisms remain unclear. Here, field excitatory postsynaptic potentials (fEPSP) recordings were made in the CA1 region of mouse hippocampal slices. The medium of APP-expressing CHO cells, which contain soluble forms of Abeta including small oligomers, inhibited LTP and facilitated long-term depression (LTD), thus making the LTP/LTD curve shift toward the right. This phenomenon could be mimicked by the non-selective glutamate transporter inhibitor, DL-TBOA. More specifically, the Abeta impaired LTP and facilitated LTD were occluded by the selective astrocytic glutamate transporter inhibitors, TFB-TBOA. In cultured astrocytes, the Abeta oligomers also decrease astrocytic glutamate transporters (EAAT1, EAAT2) expression. We conclude that soluble Abeta oligomers decrease the activation of astrocytic glutamate transporters, thereby impairing synaptic plasticity. |
