The NO/cGMP pathway inhibits transient cAMP signals through the activation of PDE2 in striatalneurons - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Frontiers in Cellular Neuroscience Année : 2013

The NO/cGMP pathway inhibits transient cAMP signals through the activation of PDE2 in striatalneurons

Résumé

The NO-cGMP signaling plays an important role in the regulation of striatal function although the mechanisms of action of cGMP specifically in medium spiny neurons (MSNs) remain unclear. Using genetically encoded fluorescent biosensors, including a novel Epac-based sensor (EPAC-S-H150) with increased sensitivity for cAMP, we analyze the cGMP response to NO and whether it affected cAMP/PKA signaling in MSNs. The Cygnet2 sensor for cGMP reported large responses to NO donors in both striatonigral and striatopallidal MSNs, this cGMP signal was controlled partially by PDE2. At the level of cAMP brief forskolin stimulations produced transient cAMP signals which differed between D-1 and D-2 MSNs. NO inhibited these cAMP transients through cGMP-dependent PDE2 activation, an effect that was translated and magnified downstream of cAMP, at the level of PKA. PDE2 thus appears as a critical effector of NO which modulates the post-synaptic response of MSNs to dopaminergic transmission.

Dates et versions

hal-01545405 , version 1 (22-06-2017)

Identifiants

Citer

Marina Polito, Jeffrey Klarenbeek, Kees Jalink, Daniele Paupardin-Tritsch, Pierre Vincent, et al.. The NO/cGMP pathway inhibits transient cAMP signals through the activation of PDE2 in striatalneurons. Frontiers in Cellular Neuroscience, 2013, 7, pp.UNSP 211. ⟨10.3389/fncel.2013.00211⟩. ⟨hal-01545405⟩
30 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More