Abstracts

Rationale: Trigeminal nerve stimulation has been shown to reduce seizure activity in both animal models and in humans. However, the mechanism by which this occurs is unknown. A fundamental question is: How do neurons in the somatosensory neocortex respond to the high frequency trigeminal stimulation that has been shown to be necessary for the anti-seizure effect? Methods: In this study, we recorded from multiple single neurons simultaneously in the primary somatosensory cortex of awake rats using arrays of chronically implanted microwire electrodes. We also implanted a nerve cuff electrode on the infraorbital branch of the trigeminal nerve contralateral to the recording site. Unimodal pulses were provided to the infraorbital nerve with current values ranging from 1-9 mA and at frequencies of 1-100 Hz. Results: Trigeminal nerve stimulation reduced the firing of single neurons in a frequency-dependent manner, with maximal firing reduction at frequencies of 62.5 Hz and above. This effect was not greatly dependent on stimulus intensity throughout the current range tested. Each pulse to the infraorbital nerve was followed by a short latency (approximately 7 ms) excitatory response, followed by a period of post-stimulus inhibition. Conclusions: These results suggest that therapeutic levels of trigeminal nerve stimulation may exert their effect in part by suppressing neuronal firing using intrinsic cortical inhibitory mechanisms. These findings have implications for the use of trigeminal nerve stimulation as a treatment for epilepsy.