Abstract:
: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 α-synuclein (α-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 α-syn interacts with and modulates synapsin III. The absence of α-syn causes a selective increase and redistribution of synapsin III, and changes the organization of synaptic vesicle pools in dopamine neurons. In α-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 α-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 α-syn and synapsin III in the regulation of dopamine neuron synaptic function.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Zaltieri M,Grigoletto J,Longhena F,Navarria L,Favero G,Castrezzati S,Colivicchi MA,Della Corte L,Rezzani R,Pizzi M,Benfenati F,Spillantini MG,Missale C,Spano P,Bellucci Adoi
10.1242/jcs.157867subject
Has Abstractpub_date
2015-07-01 00:00:00pages
2231-43issue
13eissn
0021-9533issn
1477-9137pii
jcs.157867journal_volume
128pub_type
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