Magnocellular neurons in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) secrete oxytocin not only from nerve terminals in the posterior pituitary, but also from their dendrites in the hypothalamus. These neurones are the major source of oxytocin in the brain as very large amounts of oxytocin can be released within the SON, and this can occur independently of release from nerve terminals. Because of the long half-life of peptides in the brain, it is likely that oxytocin released from neuronal dendrites within the hypothalamus can diffuse through the brain over considerable distances to reach some of the many different target sites that express high-affinity receptors for oxytocin(1). In the brain, oxytocin is involved in many behaviours, including sexual and feeding behaviours. Research on appetite has progressed rapidly in the last ten years, but there is still little understanding of how appetite-related signals are processed in the brain in vivo. During feeding, peripheral signals that inform our brain about metabolic status are integrated by peptidergic neurones in the hypothalamus and brainstem. This information is relayed to “satiety centres”, especially the ventromedial nucleus of the hypothalamus (VMH), and to the arcuate nucleus, where alpha-melanocyte-stimulating hormone (α-MSH), a potent inhibitor of food intake, is produced. The SON oxytocin cells are a target for α-MSH. We showed recently that α-MSH triggers Fos expression in SON oxytocin cells. However, surprisingly, α-MSH inhibits the electrical activity of oxytocin cells; this is mediated by endocannabinoids as CB1 cannabinoid receptor antagonist blocks the inhibitory effect of α-MSH. Remarkably, although α-MSH inhibits oxytocin cells, it stimulates oxytocin release from dendrites, this release occurs because α-MSH triggers a rise in intracellular [Ca2+] by mobilising intracellular Ca2+ stores(2,3). Centrally, both α-MSH and oxytocin inhibit food intake. It is possible therefore that the appetite-inhibiting effects of α-MSH are, at least in part, mediated by dendritically-released oxytocin. If so, a likely target for oxytocin is the VMH, which contains a high density of oxytocin receptors, and is a well-established “satiety centre”. To investigate whether oxytocin affects the electrical activity of VMH neurones in vivo, we need to identify the various types of VMH neurones by their electrical characteristics, as there is very little known about the behaviour of these neurones in vivo. In current in vivo electrophysiological experiments, we expose the ventral surface of the brain by transpharyngeal surgery and make extracellular recordings of single VMH neurons. A cannula is inserted ventrally into the third ventricle to allow central injection of oxytocin. So far, of 150 spontaneously active VMH neurones recorded, most (about 80%) are within 6 clearly distinct subpopulations of VMH neurones according to their distinctive, spontaneous firing patterns, such as the mean firing rate, interspike-interval distribution. Each of these subpopulations is then further characterised by its responses to oxytocin injected centrally via the third ventricle, and also to appetite-related peptides such as leptin, cholecystokinin (CCK), and GHRP6 (Growth Hormone Releasing Peptide 6) injected intravenously. Surprisingly, CCK although it potently inhibits feeding, has an inhibitory effect on most VMH neurones while oxytocin seems to either activate, or inhibit, or has no effect, depending on the neuronal subtype recorded.