Abstract:
:Synapsin is a synaptic vesicle-associated protein implicated in the regulation of vesicle trafficking and transmitter release, but its role in heterosynaptic plasticity remains elusive. Moreover, contradictory results have obscured the contribution of synapsin to homosynaptic plasticity. We previously reported that the neuromodulator serotonin (5-HT) led to the phosphorylation and redistribution of Aplysia synapsin, suggesting that synapsin may be a good candidate for the regulation of vesicle mobilization underlying the short-term synaptic plasticity induced by 5-HT. This study examined the role of synapsin in homosynaptic and heterosynaptic plasticity. Overexpression of synapsin reduced basal transmission and enhanced homosynaptic depression. Although synapsin did not affect spontaneous recovery from depression, it potentiated 5-HT-induced dedepression. Computational analysis showed that the effects of synapsin on plasticity could be adequately simulated by altering the rate of Ca(2+)-dependent vesicle mobilization, supporting the involvement of synapsin not only in homosynaptic but also in heterosynaptic forms of plasticity by regulating vesicle mobilization.
journal_name
J Neurophysioljournal_title
Journal of neurophysiologyauthors
Fioravante D,Liu RY,Netek AK,Cleary LJ,Byrne JHdoi
10.1152/jn.00604.2007subject
Has Abstractpub_date
2007-12-01 00:00:00pages
3568-80issue
6eissn
0022-3077issn
1522-1598pii
00604.2007journal_volume
98pub_type
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journal_title:Journal of neurophysiology
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