RT Journal Article
SR Electronic
T1 Differential cAMP Signaling at Hippocampal Output Synapses
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 14358
OP 14362
DO 10.1523/JNEUROSCI.4973-08.2008
VO 28
IS 53
A1 Wozny, Christian
A1 Maier, Nikolaus
A1 Fidzinski, Pawel
A1 Breustedt, Jörg
A1 Behr, Joachim
A1 Schmitz, Dietmar
YR 2008
UL http://www.jneurosci.org/content/28/53/14358.abstract
AB cAMP is a critical second messenger involved in synaptic transmission and synaptic plasticity. Here, we show that activation of the adenylyl cyclase by forskolin and application of the cAMP-analog Sp-5,6-DCl-cBIMPS both mimicked and occluded tetanus-induced long-term potentiation (LTP) in subicular bursting neurons, but not in subicular regular firing cells. Furthermore, LTP in bursting cells was inhibited by protein kinase A (PKA) inhibitors Rp-8-CPT-cAMP and H-89. Variations in the degree of EPSC blockade by the low-affinity competitive AMPA receptor-antagonist γ-d-glutamyl-glycine (γ-DGG), analysis of the coefficient of variance as well as changes in short-term potentiation suggest an increase of glutamate concentration in the synaptic cleft after expression of LTP. We conclude that presynaptic LTP in bursting cells requires activation of PKA by a calcium-dependent adenylyl cyclase while LTP in regular firing cells is independent of elevated cAMP levels. Our results provide evidence for a differential role of cAMP in LTP at hippocampal output synapses.