Published: 30 January, 2017 | Volume 1 - Issue 1 | Pages: 001-006
Role of Ca2+/cAMP signaling interaction in the neurotransmission. In studies published in 2013, 2015 and 2016 (Caricati-Neto et al. 2015; Bergantin et al. 2013 2015 and 2016 a,b,c,d), we discovered that the paradoxical hyperactivity of sympathetic neurons produced by L-type CCBs results of its interference on the Ca2+/cAMP signaling interaction involved in the neurotransmitter release. The pharmacological manipulation of the Ca2+/cAMP interaction by combined use L-type CCBs and cAMP-enhancer compounds could be a new therapeutic strategy for increasing central serotoninergic and monoaminergic neurotransmission in depression. cAMP: cyclic adenosine monophosphate; ATP: adenosine trisphosphate; L-, N-, P/Q-type Ca2+ channels, IP3R: Inositol trisphosphate receptor; PDE: phosphodiesterase; RyR: ryanodine receptors; SERCA: sarco-endoplasmic Ca2+-ATPase. In addition, store-operated calcium entry (SOCE) is a ubiquitous Ca2+ entry pathway that is activated in response to depletion of Endoplasmic Reticulum-Ca2+ stores, and critically controls the regulation of physiological functions in cell types.