Loss of cardiac vagal tone is a feature of many cardiovascular disorders including heart failure. The cardiac ganglia are an important potential site for regulation of vagal drive to the heart, where loss of transmission may translate to loss of vagal tone: this has been shown in a heart failure model (1). However, how cardiac vagal postganglionic neurones (CVNs) process ongoing and reflex activity has hitherto been difficult to investigate. We recently characterised CVN responses to a number of cardiorespiratory reflexes (2), and now extend this work to include the von Bezold-Jarisch reflex (vBJR), a vagally-mediated, cardioprotective reflex activated during myocardial ischaemia. Male Wistar rats (P18-25, n=12) were anaesthetised with 5% Halothane (until decerebration) for surgical set up of the working heart-brainstem preparation. The atria were opened, stabilised and the cardiac vagal ganglia exposed (2). Intracellular recordings were made from CVNs with sharp electrodes (65-140MΩ, 0.5M KCl), and classified as tonic or phasic firing neurones depending on their response to depolarising pulses (220ms, 1Hz, 1nA). CVN responses to activation of chemo- (50μl, 0.03% NaCN i.a.), baro- (+20-50mmHg), diving (100μl, ~10°C ACSF to the nose) and vBJR activation with phenylbiguanide (PBG, 200μg ia) were assessed. vBJR activation produced robust bradycardias (-84±27 bpm, n=14). Intracellular recordings were made from 14 CVNs (10 phasic, 4 tonic). All tonic cells had spontaneous EPSPs and 1 had spontaneous action potentials. vBJR and chemoreflex responses were recorded in all 4 tonic cells, on 3 of which other reflexes were also tested. All tonic cells exhibited augmented EPSP and/or spike rates in response to chemo- (+7±4Hz, n=4), baro- (+8±4 Hz, n=3), diving (+13±1 Hz, n=2) and vBJR (+16±10 Hz, n=4) activation. Notably, the increase in EPSP/spike frequency was ~2.5x higher during the vBJR than the chemoreflex despite similar bradycardias (-98±29 vs -98±35bpm). Intense vBJR activation could also produce a distinctive pattern with a depolarising envelope of summating EPSPs. Reflex activation had no effect upon phasic cells (putative interneurones). PBG produced no change in EPSP frequency in preparations that had lost brainstem reflex function, and there was no evidence of direct depolarisation or activation of local cardiac ganglionic circuits. These data show that vBJR activation excites a common pool of vagal postganglionic neurones shared with the other tested cardiorespiratory reflexes. We found no evidence of recruitment of ganglionic interneurones, nor for direct effects of PBG on the ganglion cells. The striking pattern of excitation of CVN by vBJR activation means that the intrinsic integrative properties of the ganglion cells are likely to be important in determining the magnitude of the end organ response.