Research on neuronal mechanism of trigeniinal neuropathic pain in awake behaving monkeys

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We developed the animal model with neuropathic pain using awake behaving monkeys to evaluate the neuronal mechanism of abnormal pain sensation following peripheral nerve injury. We introduced capsaicin to monkeys as the peripheral nerve irritant topically applied to the face. First, monkeys were trained to be sitting in the monkey chair quietly for 2-3 hours. After that, monkeys were trained with thermal and light detection tasks. The thermal probe was placed on the face just lateral to the nose. When monkeys pressed the button placed in front of them, temperature shift was applied from 38 to 45-47℃ (T1) for heat trials and 30-25℃ (T1) for cold trials. After 4-8 seconds hold time, small temperature shift (T2, heat trials : 0.2-0.8℃ ; cold trials : -0.5-1.0) was coming over the T1. When monkeys detected the change in this small temperature shift, they release the button and they get reword. After completion of training of these trials, monkeys were treated with capsaicin (0.04M). One hour after capsaicin treatment, monkeys were trained with same tasks to those without capsaicin. The detection latency was significantly shorter after capsaicin treatment. The primary somatosensory cortical (SI) neuronal activity was also significantly larger in monkeys treated with capsaicin as compared with untreated normal monkeys at T1 temperature of 44℃. The relationship between detection latency and SI neuronal activity were not proportional at T1 temperature of 46-47℃. We also obtained cold sensitive neurons from SI. Cold sensitive neurons we recorded so far reduced firing frequency during performing of the cold detection tasks. These cold sensitive neurons decrease firing frequency during performing of the light detection and heat detection trials as well. These suggest that some SI neurons would be involved in the detection of the on and off-sets of the stimuli with different modalities.