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

高浓度丁卡因阻滞治疗三叉神经痛是一种安全有效的方法。这一发现得到了当前感知阈值测量获得的临床数据的支持。正电子发射地形图研究表明，在伤害性刺激后，脑岛和次级躯体感觉皮层的血流量增加。这种增强被一种特定的血清素摄取抑制剂抑制。局部麻醉剂，包括丁卡因，诱导生长锥塌陷的浓度和暴露时间依赖。多种神经营养因子（如GDNF、BDNF、NT-3）加速了崩溃后的恢复。丁卡因（1-2 mM）引起生长锥内Ca^<2+>浓度升高。Ca^<2+>热点由外周向胞体向神经突内扩展。丁卡因即使在不含Ca^<2+>的培养基中也能引起生长锥塌陷。普通Ca^<2+>通道抑制剂和细胞内Ca^<2+>螯合剂略微延迟了1mM丁卡因诱导的生长锥塌陷的开始。对术后疼痛大鼠模型进行的微透析研究表明，血清素在局部释放，是有害刺激的主要原因。脊髓下降抑制通路以5 -羟色胺为神经递质，由毒蕈碱乙酰胆碱受体介导。另一个大鼠开胸后疼痛模型表明脊髓后角神经元在腰椎神经性疼痛模型中起重要作用。

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.