This is a review of our current knowledge about the role of the periaqueductal grey (PAG) in vocal control. It shows that electrical stimulation of the PAG can evoke species-specific calls with short latency and low habituation in many mammals. The vocalization-eliciting region contains neurones the activity of which is correlated with the activity of specific laryngeal muscles. Lesioning studies show that destruction of the PAG and laterally bordering tegmentum can cause mutism without akinesia. Neuroanatomical studies reveal that the PAG lacks direct connections with the majority of phonatory motoneurone pools but is connected with the periambigual reticular formation, an area which does have direct connections with all phonatory motor nuclei. The PAG receives a glutamatergic input from several sensory areas, such as the superior and inferior colliculi, solitary tract nucleus and spinal trigeminal nucleus. Glutamatergic input, in addition, reaches it from numerous limbic structures the stimulation of which also produces vocalization, such as the anterior cingulate cortex, septum, amygdala, hypothalamus and midline thalamus. Pharmacological blocking of this glutamatergic input causes mutism. The glutamatceptive vocalization-controlling neurones are under a tonic inhibitory control from GABAergic neurones. Removal of this inhibitory input lowers the threshold for the elicitation of vocalization by external stimuli. A modulatory control on vocalization threshold is also exerted by glycinergic, opioidergic, cholinergic, histaminergic and, possibly, noradrenergic and dopaminergic afferents. It is proposed that the PAG serves as a link between sensory and motivation-controlling structures on the one hand and the periambigual reticular formation coordinating the activity of the different phonatory muscles on the other.