Intracellular signal transduction and axonal transport after nerve injury, and during nerve regeneration.

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Trigeminal nerve block with a high concentration tetracaine was found effective and safe for trigeminal neuralgia. This finding was supported by clinical data obtained with current perception threshold measurements. Studies with positron emission topography demonstrated augmented blood flow in pre-cingrate cortex, insula and secondary somatic sensory cortex after a nociceptive stimulation. This augmentation was suppressed by a specific serotonin uptake inhibitor. Local anesthetics, including tetracaine, induced growth cone collapse both concentration and exposure time dependently. Recovery after the collapse was accelerated by several neurotrophic factors, such as GDNF,BDNF,NT-3. Tetracaine (1-2 mM) induced elevation in intra-growth cone Ca^<2+> concentration. The Ca^<2+> hot spot was expanded into the neurite from periphery towards cell body. Tetracaine induced growth cone collapse even in the culture media, which did not contain Ca^<2+>. A general Ca^<2+> channel inhibitor and an intracellular Ca^<2+> chelator slightly delayed the initiation of growth cone collapse induced by 1mM tetracaine. Studies with micro-dialysis in a rat model of post-operative pain showed serotonin was released locally and was a primary cause of the noxicious stimulation. Discending inhibitory pathway in spinal cord, which uses serotonin as the neurotransmitter, was mediated by muscarinic acetylcholine receptor. Another rat model of post-thoracotomy pain indicated posterior horn neurons in the spinal cord are playing important roles as in the lumbar nuropathic pain model.