| First Author | Liu S | Year | 2004 |
| Journal | EMBO J | Volume | 23 |
| Issue | 22 | Pages | 4506-16 |
| PubMed ID | 15510220 | Mgi Jnum | J:94390 |
| Mgi Id | MGI:3512696 | Doi | 10.1038/sj.emboj.7600451 |
| Citation | Liu S, et al. (2004) alpha-Synuclein produces a long-lasting increase in neurotransmitter release. EMBO J 23(22):4506-16 |
| abstractText | Wild-type alpha-synuclein, a protein of unknown function, has received much attention because of its involvement in a series of diseases that are known as synucleinopathies. We find that long-lasting potentiation of synaptic transmission between cultured hippocampal neurons is accompanied by an increase in the number of alpha-synuclein clusters. Conversely, suppression of alpha-synuclein expression through antisense nucleotide and knockout techniques blocks the potentiation, as well as the glutamate-induced increase in presynaptic functional bouton number. Consistent with these findings, alpha-synuclein introduction into the presynaptic neuron of a pair of monosynaptically connected cells causes a rapid and long-lasting enhancement of synaptic transmission, and rescues the block of potentiation in alpha-synuclein null mouse cultures. Also, we report that the application of nitric oxide (NO) increases the number of alpha-synuclein clusters, and inhibitors of NO-synthase block this increase, supporting the hypothesis that NO is involved in the enhancement of the number of alpha-synuclein clusters. Thus, alpha-synuclein is involved in synaptic plasticity by augmenting transmitter release from the presynaptic terminal. |
