Central noradrenaline (NA) release impacts on many vital physiological functions, for example blood pressure control (Duale et al. 2005). In order to understand the mechanisms regulating NA secretion in the brain, we need to characterise vesicle fusion events in central noradrenergic (NAergic) neurones. In addition, it was previously uncertain whether NA release occurs only from varicosities or also from soma and dendrites, although the distribution of release sites is the key determinant for the impact of secreted NA in the brain. Indeed, while release from axonal terminals will activate receptors in target areas, somato-dendritic release may result in autoinhibition of NAergic neurones and affect adjacent interneurones within NAergic nuclei. Microamperometry was used to directly measure release from NAergic neurones expressing enhanced green fluorescent protein in organotypic brainstem slice cultures (Teschemacher, 2004; Teschemacher et al. 2005). Oxidation spikes were registered at a driving voltage of +800 mV using stiff carbon fibre microelectrodes (active surface tip diameter ~5 μm) which were placed onto green fluorescent somata or axonal varicosities of NAergic neurones. Our data suggest NA release from two major populations of secretory vesicles. The main population of events measures median (±s.e.m.) values for amperometric charge: 0.04 ±0.004 pCoulomb; amplitude: 8.3 ±0.5 pA; and half time: 3.2 ±0.14 ms (n=16). These properties are not significantly different between somato-dendritic and axonal release sites. Spike frequencies vary widely between individual release sites but, again, are not significantly different between the somato-dendritic compartment and axons. Assuming that intravesicular NA concentration in central neurones is comparable to that proposed for adrenal chromaffin cells, these results suggest that the majority of NA-secreting vesicles in the brain are small with diameters ranging around 75 nm, consistent with electron microscopy data (Bloom & Aghajanian, 1968; Travis & Wightman, 1998). In addition, at about 25% of release sites, we also registered large release events consistent with vesicle diameters of 300-400 nm. While these events represented only about 5% of the total spike population, due to their high charge, they contributed about 25% to the total NA release registered at these sites. The majority (~80%) of the large events was registered at axonal release sites. We conclude that exocytosis occurs from both, axonal varicosities and the somato-dendritic compartments, of central NAergic neurones. Our data further suggest that some axonal release sites may, in addition, utilise very large vesicles which appear comparable to adrenal chromaffin cell granules.