Lay summary
After a heart attack, inappropriate activation of the sympathetic nerves that innervate the heart can cause the heart to ‘skip’ a beat (arrhythmia), which is a leading cause of death. We have found that specific oxytocin neurons within the brain are activated immediately after a heart attack, and further shown that these neurons project to the brain regions from where the sympathetic nerves originate. Therefore, to definitively show that these oxytocin neurons are instrumental in activating the sympathetic nerves, we will use in vivo fluorescence photometry to selectively visualise activation of oxytocin neurons at the precise time of a heart attack, with which we can then correlate with changes in sympathetic traffic to the heart. Importantly, we further aim to show that pharmacological blockade of these oxytocin cells can prevent over-stimulation of the failing heart and, thus, identify a novel therapeutic target for the management of heart attacks.