Alterations of neuronal response and transcription factors in the trigeminal nucleus following deafferentation pain

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This study has been conducted to investigate the mechanisms of development of deafferentation pain including allodynia and hyperalgesia. (1) Neuropathic surgery for animal model : The induction of deafferentation pain was achieved by extraction of the left upper and lower incisor teeth or loose ligation of the inferior alveolar nerve with a chromic gut suture. Mechanical stimulation was applied within the surface of skin around whisker and cheek, sensory of which is controlled by the trigeminal nerves. As an indicator of deafferentation pain, the development of allodynia was determined by von Frey filaments. Tactile allodynia developed by day 7 after the nerve injury and lasted for at least 3 weeks. (2) Mechanisms on development of tactile allodynia : (1) Behavioral experiment : Tactile allodynia was recovered by administration of carbamazepine, N^G-monomethyl-L-arginine (L-NMMA ; nitric oxide (NO) synthase inhibitor) and MK-801 in dosedependent manner. (2) Electrophysiological experiment : The alteration of NO current evoked by the i.v. administration of N-methyl-D-aspartate (NMDA) and MK801 was significantly larger in the ipsilateral side of the superficial layers of the trigeminal nucleus caudalis of operated rats than that of control animals. (3) Immunohistochemical experiment : The number of NO synthase (NOS)-positive neurons were measured in the trigeminal nucleus caudalis. The number of nNOS-positive neurons increased in the layers I-II and III-IV in both side (ipsilateral and contralateral) of operated animals. These results suggest that allodynia developed following dental peripheral nerve injury, and NMDA/NO pathways may be involved in development of tactile allodynia. Crrently we investigate what signal transduction pathways and transcription factors are involved in development of such tactile allodynia. (259 words)