Effects of electromagnetic millimeter waves on the neuron activity of the spinal trigeminal nucleus of the rat

The study examined the effects of continuous low-intensity electromagnetic millimeter waves (MMW; frequency 40 GHz, power density of 0.04 mW/cm2) on ongoing firing of the spinal trigeminal nucleus (STN) neurons and their responses to the electrical stimulation of the dura mater in neurophysiological experiments on anesthetized rats. It is known that local exposure of MMW to certain areas of the skin can have a systemic therapeutic effect in the treatment of various pathologies. In particular, it concerns the use of MMW to treat headache of different genesis, with migraine being the most common form. The mechanisms of migraine are not clear, but it is known that the STN plays a key role in the migraine pathogenesis, providing the primary processing of pain signals from the cranial vessels as well as the transmission of these signals to overlying brain structures, in particular, to the thalamus. Recently, it has been reported that the frequency-modulated MMW causes short-term inhibitory changes in both the background activity of STN neurons and their responses to electrical stimulation of the dura mater. We assumed that the use of MMW in the unmodulated mode will allow to increase the duration of the MMW inhibitory effect on the background and evoked activity of STN neurons and thereby confirm potential antinociceptive action of MMW in migraine. The results of the present study have showed that the exposure of the STN neurons’ cutaneous receptive fields to unmodulated MMW is accompanied by prolonged cumulative inhibition of both the background activity of these neurons and their dural electrostimulation-evoked responses. The data allow considering these effects as an evindence in favour of potential antimigraine action of a continuous low-intensity MMW. It is proposed that the action can be based on the activation of nervous and immune processes in the skin, which, through a chain of neuronal mechanisms, can lead to a decrease in the excitability of STN neurons involved in the pathogenesis of migraine.