PT  - JOURNAL ARTICLE
AU  - Wozny, Christian
AU  - Maier, Nikolaus
AU  - Fidzinski, Pawel
AU  - Breustedt, Jörg
AU  - Behr, Joachim
AU  - Schmitz, Dietmar
TI  - Differential cAMP Signaling at Hippocampal Output Synapses
AID  - 10.1523/JNEUROSCI.4973-08.2008
DP  - 2008 Dec 31
TA  - The Journal of Neuroscience
PG  - 14358--14362
VI  - 28
IP  - 53
4099  - http://www.jneurosci.org/content/28/53/14358.short
4100  - http://www.jneurosci.org/content/28/53/14358.full
SO  - J. Neurosci.2008 Dec 31; 28
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.