Discover the role of Ca2+/Camp signal interactions in neurotransmission and neuroprotection: their contribution to the treatment of neurological and psychiatric diseases

Abstract

Our discovery of the interaction between Ca2+ and cAMP-mediated intracellular signaling pathways (Ca2+/
cAMP interaction) in neurotransmission and neuroprotection is of great significance for understanding the cellular and
molecular mechanisms involved in the pathogenesis of neurological and psychiatric diseases . , Alzheimer's disease and
Parkinson's disease and other diseases. Interestingly, this discovery appeared decades ago, when hypertensive patients
reported that the use of L-type Ca2+ channel blockers (CCB) can reduce arterial pressure, but exhibits typical
symptoms of sympathetic hyperactivity. For example, tachycardia and elevated plasma catecholamine levels. Although
CCB has these adverse effects, although it was originally thought that its purpose is to regulate the arterial pressure
reflex, this mysterious phenomenon called the "calcium paradox" has been unclear for the past 40 years. In 2013, we
discovered that this phenomenon is caused by the increase in transmitter emission of sympathetic neurons and adrenal
chromaffin cells stimulated by CCB by interfering with the Ca2+/cAMP interaction. In this way, our discovery of the
role of Ca2+/cAMP interaction in neurotransmitter release and neuronal cell death induced by cytoplasmic Ca2+
overload is of great significance for the development of new pharmacological strategies for more effective treatment of
neurological and psychiatric diseases. Greatly. Diseases and neuronal cell death caused by insufficient neurotransmitter
release.