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Recent advances in pharmacotherapy of neurological and psychiatric disorders promoted by discovery of the role of Ca2+/cAMP signaling interaction in the neurotransmission and neuroprotection Advance Pharmaceutical Journal

Review Articles

2016  |  Vol: 1(3)  |  Issue: 3 (July- August)
Recent advances in pharmacotherapy of neurological and psychiatric disorders promoted by discovery of the role of Ca2+/cAMP signaling interaction in the neurotransmission and neuroprotection

Leandro Bueno Bergantin, PhD and Afonso Caricati-Neto, Ph.D.*

Laboratory of Autonomic and Cardiovascular Pharmacology,

Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), 55 11 5576-4973, Rua Pedro de Toledo, 669 – Vila Clementino, São Paulo – SP, Brazil, Postal Code: 04039-032.

*Corresponding Author

Dr. Afonso Caricati-Neto

Laboratory of Autonomic and Cardiovascular Pharmacology,

Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), 55 11 5576-4973, Rua Pedro de Toledo, 669 – Vila Clementino, São Paulo – SP, Brazil, Postal Code: 04039-032.

Abstract

Our discovery of the involvement of the interaction between intracellular signalling pathways mediated by Ca2+ and cAMP (Ca2+/cAMP signaling interaction) in the neurotransmission and neuroprotection has produced important advances in the understanding of the pathophysiology and pharmacology of neurological and psychiatric disorders, such as Alzheimer´s and Parkinson's diseases. Interestingly, this discovery initiated decades ago when numerous clinical studies have reported that L-type Ca2+ channel blockers (CCBs) used in antihypertensive pharmacotherapy decreased arterial pressure, but produced typical symptoms of sympathetic hyperactivity such as tachycardia and increment of catecholamine plasma levels. Despite these adverse effects of CCBs have been initially attributed to adjust reflex of arterial pressure, during almost four decades this enigmatic phenomenon named "calcium paradox" remained unclear.  In 2013, we discovered that these "calcium paradox" results of transmitter release from sympathetic neurons and adrenal chromaffin cells stimulated by CCBs due to its modulatory action on the Ca2+/cAMP signaling interaction. In addition, we discovered that this modulatory action attenuates neuronal death triggered by cytosolic Ca2+ overload. These findings open a large avenue for the development of new pharmacological strategies more effective for the treatment of neurological and psychiatric disorders resulting of neurotransmitter release deficit, and neuronal death.

Keywords: Ca2+/cAMP signaling interaction; neurotransmission; neuroprotection; neurological/psychiatric disorders

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