| First Author | Di Prisco S | Year | 2012 |
| Journal | J Neurochem | Volume | 121 |
| Issue | 3 | Pages | 428-37 |
| PubMed ID | 22385043 | Mgi Jnum | J:184479 |
| Mgi Id | MGI:5424085 | Doi | 10.1111/j.1471-4159.2012.07720.x |
| Citation | Di Prisco S, et al. (2012) RANTES-mediated control of excitatory amino acid release in mouse spinal cord. J Neurochem 121(3):428-37 |
| abstractText | The impact of Regulated upon Activation Normal T cells Expressed and Secreted (RANTES) on the release of pre-loaded [(3)H]D-aspartate ([(3)H]D-ASP) from mouse spinal cord synaptosomes was investigated. RANTES (0.01-1 nM) failed to affect the spontaneous release, but facilitated the 15 mM K(+)-evoked overflow of [(3)H]D-ASP. Incubation of synaptosomes with antibodies raised against the chemokine receptor (CCR)1 and CCR5 proteins prevented RANTES-induced facilitation of glutamate exocytosis, whereas anti-CCR3 antibody was inefficacious. Accordingly, BX513 and D-Ala-peptide T-amide (DAPTA) CCR1 and CCR5 antagonists, respectively, prevented RANTES-induced effect, whereas the CCR3 antagonist SB 328437 was inactive. To compare these findings to previous results, we quantified the effects of CCR antagonists on the RANTES-induced modifications of the spontaneous and the K(+)-evoked [(3)H]D-ASP release in the mouse cortex. Here, CCR1 and CCR5, but not CCR3, antagonists prevented the RANTES-mediated [(3)H]D-ASP release, whereas RANTES-induced inhibition of the 12 mM K(+)-evoked [(3)H]D-ASP exocytosis was also antagonized by SB 328437. Facilitation of glutamate exocytosis in spinal cord relied on PLC-dependent mobilization of Ca(2)(+) from IP(3)-sensitive stores; adenylyl cyclase was not involved. CCR1, CCR3 and CCR5 receptor proteins were present in spinal cord synaptosomal and gliosomal lysates, although RANTES-induced changes to glutamate release could not be observed in gliosomes. Our results confirm the role of RANTES as modulator of glutamate transmission. |
