| First Author | Zaltieri M | Year | 2015 |
| Journal | J Cell Sci | Volume | 128 |
| Issue | 13 | Pages | 2231-43 |
| PubMed ID | 25967550 | Mgi Jnum | J:232828 |
| Mgi Id | MGI:5780271 | Doi | 10.1242/jcs.157867 |
| Citation | Zaltieri M, et al. (2015) alpha-synuclein and synapsin III cooperatively regulate synaptic function in dopamine neurons. J Cell Sci 128(13):2231-43 |
| abstractText | The main neuropathological features of Parkinson's disease are dopaminergic nigrostriatal neuron degeneration, and intraneuronal and intraneuritic proteinaceous inclusions named Lewy bodies and Lewy neurites, respectively, which mainly contain alpha-synuclein (alpha-syn, also known as SNCA). The neuronal phosphoprotein synapsin III (also known as SYN3), is a pivotal regulator of dopamine neuron synaptic function. Here, we show that alpha-syn interacts with and modulates synapsin III. The absence of alpha-syn causes a selective increase and redistribution of synapsin III, and changes the organization of synaptic vesicle pools in dopamine neurons. In alpha-syn-null mice, the alterations of synapsin III induce an increased locomotor response to the stimulation of synapsin-dependent dopamine overflow, despite this, these mice show decreased basal and depolarization-dependent striatal dopamine release. Of note, synapsin III seems to be involved in alpha-syn aggregation, which also coaxes its increase and redistribution. Furthermore, synapsin III accumulates in the caudate and putamen of individuals with Parkinson's disease. These findings support a reciprocal modulatory interaction of alpha-syn and synapsin III in the regulation of dopamine neuron synaptic function. |
