Inhibition of PDE2A, but not PDE9A, modulates presynaptic short‐term plasticity measured by paired‐pulse facilitation in the CA1 region of the hippocampus

In conclusion, these data provide new evidence supporting a role of PDE2A modulating short‐term synaptic plasticity. Moreover, this function of PDE2A is suggested to rely on an active modulation of the cAMP hydrolysis as a response to changes in cGMP levels at the presynaptic level. We studied the functional location of phosphodiesterases (PDE) 2A and 9A. Activation of soluble guanylyl cyclase with BAY 41‐8543 impaired the forskolin‐induced increase in basal transmission and decrease in PPF. While PDE9A inhibitor did not change this forskolin effect on PPF, inhibition of PDE2A potentiated it, suggesting its presynaptic location. This article is protected by copyright. All rights reserved. We studied the functional location of phosphodiesterases (PDE) 2A and 9A. Activation of soluble guanylyl cyclase with BAY 41‐8543 impaired the forskolin‐induced increase in basal transmission and decrease in PPF. While PDE9A inhibitor did not change this forskolin effect on PPF, inhibition of PDE2A potentiated it, suggesting its presynaptic location.
Source: Synapse - Category: Neurology Authors: Tags: Research Article Source Type: research