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

神经损伤后和神经再生过程中的细胞内信号转导和轴突运输。

基本信息

批准号：
14370481
负责人：
GOTO Fumio
金额：
$ 9.41万
依托单位：
Gunma University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

项目摘要

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.

高浓度丁卡因三叉神经阻滞治疗三叉神经痛安全有效。这一发现得到了用当前知觉阈值测量获得的临床数据的支持。正电子发射地形图的研究表明，伤害性刺激后，前扣带回皮质、脑岛和次级躯体感觉皮质的血流量增加。这种增强被一种特定的5-羟色胺摄取抑制剂抑制。包括丁卡因在内的局麻药可诱导生长锥塌陷，且呈浓度和暴露时间依赖性。GDNF、BDNF、NT-3等神经营养因子可加速塌陷后的恢复。丁卡因(1-2 mM)可引起生长锥内钙离子浓度升高。Ca~(2+)热点由外周向胞体向突起内扩展。即使在不含Ca~(2+)和Gt~(2+)的培养液中，丁卡因也能引起生长锥的塌陷。普通钙通道阻滞剂和细胞内钙离子螯合剂对1 mM丁卡因引起的生长锥塌陷有轻微的延迟作用。对手术后疼痛的大鼠模型进行的微透析研究表明，5-羟色胺在局部释放，是有害刺激的主要原因。脊髓以5-羟色胺为神经递质的发现抑制通路是由M胆碱受体介导的。另一种开胸术后疼痛的大鼠模型表明，脊髓中的后角神经元在腰神经病理性疼痛模型中发挥着重要作用。