Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

In sympathetic neurons innervating the heart, action potentials activate voltage-gated Ca2+ channels and evoke Ca2+ entry into presynaptic terminals triggering neurotransmitter release. Binding of transmitters to specific receptors stimulates signal transduction pathways that cause changes in cardiac function. The mechanisms contributing to presynaptic Ca2+ dynamics involve regulation of endogenous Ca2+ buffers, in particular the endoplasmic reticulum, mitochondria and cyclic nucleotide targeted pathways. The purpose of this review is to summarize and highlight recent findings about Ca2+ homeostasis in cardiac sympathetic neurons and how modulation of second messengers can drive neurotransmission and affect myocyte excitability in cardiovascular disease. Moreover, we discuss the underlying mechanism of abnormal intracellular Ca2+ homeostasis and signaling in these neurons, and speculate on the role of phosphodiesterases as a therapeutic target to restore normal autonomic transmission in disease states of overactivity.

Original publication

DOI

10.1016/j.semcdb.2019.01.010

Type

Journal article

Journal

Semin Cell Dev Biol

Publication Date

23/01/2019

Keywords

Calcium, Cardiac excitability, Cyclic nucleotide, Phosphodiesterase, Sympathetic neuron