期刊
JOURNAL OF NEUROSCIENCE
卷 35, 期 16, 页码 6544-6553出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0314-14.2015
关键词
cAMP; Epac2; mossy fiber; readily releasable pool
资金
- National Institutes of Health-National Institute of Mental Health [R01MH099114]
- McKnight Foundation
- Canadian Institutes of Health Research
- institutional T32 award [T32 MH067564]
- National Institutes of Health-National Cancer Institute [P30 CA060553]
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.
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