During development of the nervous system, neural networks are massively activated in episodes of synchronized bursting. Although this activity has been shown to influence several aspects of nervous system development, there is no compelling or unifying theory concerning its function. This is probably because it is technically very difficult to isolate the developmental effects of neural activity per se from confounding factors. Perhaps for this reason, most of the recent research on developing network activity has focused on understanding the mechanisms of its generation. As a result of this work, a consensus is emerging that two properties of developing networks predispose them to become spontaneously active. The first is their hyperexcitability, which is due – in part – to the depolarizing action of the classically inhibitory neurotransmitters GABA and glycine during development. The second is a transient activity-dependent depression of network excitability that follows a burst and recovers in the interval between bursts. Modelling work has shown that these two network properties are sufficient to produce episodes of spontaneous bursting (Tabak et al. 2000). Both of these general properties are common to many developing networks and do not depend on the details of network architecture. However, network structure does influence the way activity evolves and the manner in which the various network components are recruited. For example, the somatic motoneurones of the developing chick spinal cord – normally considered the output elements of spinal networks – seem to be responsible for initiating episodes of spontaneous activity in the spinal cord. Similarly, it has recently been shown that the glutamatergic pyramidal CA3 neurones of the neonatal rat hippocampus have voltage-dependent properties that allow them to function as ‘intrinsic bursters’ that drive network activity (Sipila et al. 2005). In a new study, reported in this issue of The Journal of Physiology, Hunt et al. (2005) provide evidence that the serotonergic neurones of the raphe may play a similar initiating role in generating spontaneous activity in the hindbrain. To assess the pattern of activity, they used imaging of the E11.5 mouse brainstem loaded with the calcium indicator fluo-4. They found that neuronal calcium transients occurred spontaneously at a rate of ∼3 min−1 and were widely synchronized throughout the hindbrain. Three pieces of evidence suggested that this activity originated from the serotonergic neurones of the midline raphe system. First, the calcium transients propagated in a mediolateral direction. Second, when the medial and lateral parts of the hindbrain were surgically isolated, the calcium transients were abolished or greatly reduced in the lateral section but not in the medial section that contained the serotonergic neurones. Finally, spontaneous activity in the hindbrain was abolished by antagonists to the 5-HT2A receptor but not to any of the fast ionotropic neurotransmitters (glutamate, GABA, glycine and acetylcholine). For technical reasons it was not possible to verify directly that the midline serotonergic neurones were actually the source of this activity. However, this seems very likely given that they comprise the great majority (80%) of the midline neurones. It should be possible to test this idea definitively in mice, in which serotonergic neurones expressing the PET-1 transcription factor are marked with GFP. Spontaneous activity in the hindbrain is not completely dependent on the serotonergic raphe system because it persists in lateral sections deprived of their serotonergic input, albeit at a slower rate than in the intact hindbrain. This observation raises questions concerning the mechanisms responsible for the activity. In particular, it is not clear if the serotonergic neurones are pacemakers that drive the rest of the network or if they act more generally to increase network excitability through activation of 5-HT2A receptors. The serotonergic raphe system projects widely throughout the brain and spinal cord and its activity can influence many developing networks. Indeed, disruption of serotonergic inputs is known to produce abnormalities in the development of the spinal cord and the cortex (Norreel et al. 2003; Vitalis & Parnavelas, 2003). Although Hunt et al. (2005) only examined the activity of the hindbrain at a single stage in development (E11.5), it will be important in future studies to identify how the activity of the serotonergic raphe system changes during development and how this influences the behaviour of networks receiving raphe projections. It will also be of interest to establish the mechanism of activation of the serotonergic neurones, and in particular, whether or not they possess the voltage-dependent conductances that would endow them with intrinsic bursting capability. This will require direct intracellular recordings from identified serotonergic neurones that should be forthcoming in the near future.