Figure 1

Novel Challenges for the Therapeutics of Depression: Pharmacological Modulation of Interaction between the Intracellular Signaling Pathways Mediated by Ca2+ and cAMP

Afonso Caricati-Neto and Leandro Bueno Bergantin*

Published: 30 January, 2017 | Volume 1 - Issue 1 | Pages: 001-006

jatr-aid1001-g001

Figure 1:

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.

Read Full Article HTML DOI: 10.29328/journal.jatr.1001001 Cite this Article Read Full Article PDF

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