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- W2049370912 endingPage "3596" @default.
- W2049370912 startingPage "3583" @default.
- W2049370912 abstract "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." @default.
- W2049370912 created "2016-06-24" @default.
- W2049370912 creator A5004447815 @default.
- W2049370912 creator A5022609803 @default.
- W2049370912 creator A5032187017 @default.
- W2049370912 creator A5041283272 @default.
- W2049370912 creator A5055939275 @default.
- W2049370912 creator A5067872357 @default.
- W2049370912 date "2007-06-01" @default.
- W2049370912 modified "2023-10-16" @default.
- W2049370912 title "?-Synuclein involvement in hippocampal synaptic plasticity: role of NO, cGMP, cGK and CaMKII" @default.
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