| First Author | Fattorini G | Year | 2020 |
| Journal | Glia | Volume | 68 |
| Issue | 3 | Pages | 646-655 |
| PubMed ID | 31692106 | Mgi Jnum | J:297915 |
| Mgi Id | MGI:6479403 | Doi | 10.1002/glia.23745 |
| Citation | Fattorini G, et al. (2020) Microglial expression of GAT-1 in the cerebral cortex. Glia 68(3):646-655 |
| abstractText | Microglial cells are the immune cells of the brain that, by sensing the microenvironment, permit a correct brain development and function. They communicate with other glial cells and with neurons, releasing and responding to a number of molecules that exert effects on surrounding cells. Among these, neurotransmitters and, in particular, gamma-aminobutyric acid (GABA) has recently gained interest in this context. We demonstrated the expression of GABA transporter 1 (GAT-1) in microglial cells both in soma and cell processes. We show that microglial cell treatment with 1,2,5,6-tetrahydro-1-[2-[[(diphenylmethylene)amino]oxy]ethyl]-3-pyridinecarboxyli c acid hydrochloride (NNC-711), a potent and selective GAT-1 inhibitor, significantly reduced Na(+) -dependent GABA uptake. On the other hand, GABA uptake was significantly increased by cell treatment with (S)-1-[2-[tris(4-methoxyphenyl)methoxy]ethyl]-3-piperidinecarboxylic acid (SNAP-5114), a GAT-2/3 inhibitor, and this effect was completely blocked by the botulinum toxin BoNT/C1, that specifically cleaves and inactives syntaxin 1A (STX1A). Overall, these findings show that microglial cells express GAT-1 and indicate that STX1A plays an important role in the regulation of GAT-1-dependent GABA uptake in microglia. |
