α-Synuclein involvement in hippocampal synaptic plasticity: Role of NO, cGMP, cGK and CaMKII

Shumin Liu, Mauro Fa, Ipe Ninan, Fabrizio Trinchese, William Dauer, Ottavio Arancio

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Synaptic plasticity involves a series of coordinate changes occurring both pre- and postsynaptically, of which α-synuclein is an integral part. We have investigated on mouse primary hippocampal neurons in culture whether redistribution of α-synuclein during plasticity involves retrograde signaling activation through nitric oxide (NO), cGMP, cGMP-dependent protein kinase (cGK) and calmodulin-dependent protein kinase II. We have found that deletion of the α-synuclein gene blocks both the long-lasting enhancement of evoked and miniature transmitter release and the increase in the number of functional presynaptic boutons evoked through the NO donor, DEA/NO, and the cGMP analog, 8-Br-cGMP. In agreement with these findings both DEA/NO and 8-Br-cGMP were capable of producing a long-lasting increase in number of clusters for α-synuclein through activation of soluble guanylyl cyclase, cGK and calcium/calmodulin-dependent protein kinase IIα. Thus, our results suggest that NO, cGMP, GMP-dependent protein kinase and calmodulin-dependent protein kinase II play a key role in the redistribution of α-synuclein during plasticity.

Original languageEnglish (US)
Pages (from-to)3583-3596
Number of pages14
JournalEuropean Journal of Neuroscience
Volume25
Issue number12
DOIs
StatePublished - Jun 1 2007
Externally publishedYes

Keywords

  • Cell culture
  • Immunoreactive clusters
  • Mouse
  • Synaptic plasticity
  • Vesicle cycling

ASJC Scopus subject areas

  • Neuroscience(all)

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