Introduction Discrete regions in the heart called ganglionic plexuses (GP), primarily parasympathetic in nature, represent a network of integration centres that constitute the hearts ‘little brain’ [1]. Recent data suggest that GP are involved in the pathogenesis arrhythmias such as atrial fibrillation but the precise mechanisms are not well understood [2]. Our aims were to 1) assess the presence of parasympathetic axons and putative ganglia and 2) investigate the functional role of the right atrial GP (RAGP) in controlling heart rate (HR). Methods The decentralised isolated innervated rabbit heart was used (n=10). After sedation (ketamine, 10mg/kg; medetomidine hydrochloride, 0.2mg/kg; butorphanol, 0.05mg/kg; im) anaesthesia was achieved with propofol (1%w/v ad libitum, iv) during which the innervated heart model was prepared [3]. Animals were killed with pentobarbitone (160mg/kg, iv) and the preparation was perfused via the aorta in constant flow. Aim 1: 3 hearts were cut into regions, fixed and stained for acetylcholinesterase. A qualitative scoring system assessed axonal and putative ganglia levels. Aim 2: (n=7) a) RAGP was stimulated using 0.1-0.4mg nicotine (0.1ml), b) in the presence of 0.1μM Atropine (AT) or 1.8μM Metoprolol (Met), c) The right vagus nerve was stimulated (VNS, 7H10V) before and after RAGP stimulation and d) VNS before and following coronary artery occlusion (CAO). Data are mean±SEM, repeated measures ANOVA or Students t-test, *P<0.05 vs control. Results Aim 1) See figure. Parasympathetic axons and putative ganglia were seen in all regions studied with the highest levels seen in the right atria. There was significant levels of axons and ganglia present in the left ventricle. Aim 2) i) RAGP stimulation elicited an initial bradycardia (145±9 to 109±3bpm*) and secondary tachycardia (226±12bpm*, n=5) ii) AT abolished the bradycardia (139±8 to 138±10bpm), but not the tachycardia (247±9bpm*). Met did not affect the bradycardia (135±7 to 106±4*) but abolished the tachycardia (128±6bpm, N=5. iii) VNS-bradycardia was augmented after RAGP activation (-81±8 vs -142±9bpm*, n=3). iv) CAO increased VNS-bradycardia (-45±6 vs -68±8bpm*, n-4). Conclusion These are the first data of the presence and functional effects of GP in the rabbit. Structurally, axonal and putative GP abundance differs throughout the heart being highest at the atria but also prominent in the LV. Functionally, RAGP activation elicits a mixed autonomic HR response, via vagal and sympathetic activation that enhanced VNS-bradycardia. In addition, novel data shows that acute ventricular ischemia augments the HR effect of cervical VNS confirming that the RAGP is important in controlling HR in this species.