Abstract
Clinical observations imply that vascular compression and demyelination of the trigeminal nerve root have been major etiological factors. LPA, released after nerve injury, also induces demyelination, which may cause neuropathic pain and may increase nociceptive activity. Surgical procedures were performed under pentobarbital sodium (40 mg/kg, ip). Under anesthesia, LPA (1 nmol/ 3 µl) was injected into the left trigeminal ganglion. We examined free behavior (spontaneous pain), air-puff test (mechanical allodynia), pinprick response (mechanical hyperalgesia), and acetone test (cold allodynia) at -3, 3, 7, 10, 14, 17, 21, 24, 30, 40, 55, 70, 85, 100 and 130 days after surgery. The most obvious behavioral changes that occurred following microinjection of LPA into the trigeminal ganglion were a dramatic increase in the responses to mechanical stimulation of the face. The thresholds of air-puff significantly decreased after microinjection of LPA. In the almost LPA-treated animals, mechanical allodynia was established within 3-7 days bilaterally and strongly remained over 40 days following LPA injection. Microinjection of LPA produced mirror-image mechanical allodynia. Microinjection of LPA produced demyelination of axon in the trigeminal ganglion. These results suggest that demyelination plays a major etiological role in trigeminal neuralgia and that LPA-induced trigeminal neuralgia animal model help us study pathogenesis of trigeminal neuralgia. Supported by: grant (No. R01-2006-000-10488-0) from KSEF. [J Physiol Sci. 2007;57 Suppl:S36]
