Activation of spinal trigeminal neurons with meningeal afferent input is suggested to cause headaches. High activity of peripheral nociceptors projecting to these neurons can cause central sensitization, which may underlie chronic headaches. In electrophysiological experiments central sensitization is apparent as spontaneous activity of central neurons and hypersensitivity of innervated tissues. We investigated if spontaneous activity of neurons in the spinal trigeminal nucleus is driven from peripheral afferent input.

Experiments were performed in adult rats. Spontaneous activity was registered in Sp5O and Sp5C subnuclei of the spinal trigeminal nucleus. Receptive fields were evaluated using von Frey filaments. Sp5O neurons received peripheral input from facial areas, units in Sp5C had additional receptive fields in the exposed dura mater. Lidocaine was microinjected into V3 (for Sp5O units) and V1/V2 (for Sp5C units) divisions of the trigeminal ganglion via the infraorbital channel.

Microinjection of lidocaine but not saline was followed by a decrease in both the receptive field size and the spontaneous activity of the recorded units. Mechanical insensitivity of receptive fields was accompanied by the disappearance of spontaneous activity.

We conclude that the spontaneous activity of the neurons in spinal trigeminal nucleus depends on the peripheral afferent input.