Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 1, Pages 208-214Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3703-04.2005
Keywords
synaptic transmission; synaptic plasticity; neuromodulation; intracellular signaling; cAMP; Epac
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Glutamatergic synapses are highly modifiable, suiting them for key roles in processes such as learning and memory. At crayfish glutamatergic neuromuscular junctions, hyperpolarization and cyclic nucleotide-activated (HCN) ion channels mediate hormonal modulation of glutamatergic synapses and a form activity-dependent long-term facilitation (LTF) of synaptic transmission. Here, we show that a new target for cAMP, exchange protein activated by cAMP ( Epac) or cAMP-regulated guanine nucleotide exchange protein, is involved in the hormonal enhancement of synaptic transmission by serotonin. Induction of LTF tags synapses, rendering them responsive to cAMP in an HCN-independent manner. Epac also mediates the enhancement of tagged synapses. Thus, the cAMP-dependent enhancement of transmission is mediated by two separate pathways, neither of which involves protein kinase A.
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