| First Author | Fernandes HB | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 16 | Pages | 6544-53 |
| PubMed ID | 25904804 | Mgi Jnum | J:221665 |
| Mgi Id | MGI:5641291 | Doi | 10.1523/JNEUROSCI.0314-14.2015 |
| Citation | Fernandes HB, et al. (2015) Epac2 Mediates cAMP-Dependent Potentiation of Neurotransmission in the Hippocampus. J Neurosci 35(16):6544-53 |
| abstractText | Presynaptic terminal cAMP elevation plays a central role in plasticity at the mossy fiber-CA3 synapse of the hippocampus. Prior studies have identified protein kinase A as a downstream effector of cAMP that contributes to mossy fiber LTP (MF-LTP), but the potential contribution of Epac2, another cAMP effector expressed in the MF synapse, has not been considered. We investigated the role of Epac2 in MF-CA3 neurotransmission using Epac2(-/-) mice. The deletion of Epac2 did not cause gross alterations in hippocampal neuroanatomy or basal synaptic transmission. Synaptic facilitation during short trains was not affected by loss of Epac2 activity; however, both long-term plasticity and forskolin-mediated potentiation of MFs were impaired, demonstrating that Epac2 contributes to cAMP-dependent potentiation of transmitter release. Examination of synaptic transmission during long sustained trains of activity suggested that the readily releasable pool of vesicles is reduced in Epac2(-/-) mice. These data suggest that cAMP elevation uses an Epac2-dependent pathway to promote transmitter release, and that Epac2 is required to maintain the readily releasable pool at MF synapses in the hippocampus. |
