Activation of dural nociceptors by inflammatory agents, mechanical or thermal stimuli may result in the development of hypersensitivity and increased activity in central trigeminal neurons. It is assumed that once achieved the sensitized state and increased activity of central neurons remains independent of the peripheral nociceptive drive. To examine if increased central trigeminal activity is dependent on peripheral sensory impulses, an animal model of meningeal nociception was used. In isoflurane anesthetized rats a cranial window was made to expose the parietal dura mater. Access through the medullary brainstem allowed extracellular action potentials to be recorded from neurons in the spinal trigeminal nucleus that received afferent input from the exposed dura. Sensitivity of dural receptive fields was tested with von Frey hairs. Peripheral sensory input was blocked by local microinjection of 5% lidocaine (20 ml) into Meckel's space. Injection of lidocaine was followed by a dramatic fall in central activity and the disappearance of dural receptive fields. Recovery of peripheral conductivity was observed after 40–50 min and was followed by recovery of the central activity 60–70 min after the lidocaine injection. The results suggest that central activity requires peripheral afferent drive and that the sensitized state of central neurons may not be alone sufficient to generate impulses.