Dunnett S B
Cambridge Centre for Brain Repair, University of Cambridge, UK.
J Neurol. 1994 Dec;242(1 Suppl 1):S43-53. doi: 10.1007/BF00939242.
Neural grafts can reverse many functional deficits associated with brain damage, whether of traumatic, toxic, neurodegenerative or genetic origin. In some model systems recovery can be partial or complete; whereas in others the grafts have limited effects or may actually cause further dysfunction. In order to devise rational and effective transplantation strategies it is necessary to understand the mechanisms by which grafts exert their functional effects. Several alternatives have been proposed, and these include non-specific consequences of surgery, acute diffuse neurotrophic and growth mechanisms, chronic diffuse release of deficient neurochemicals, bridging tissues for host regeneration, diffuse reinnervation of the host brain, and reciprocal graft-host reconnection. These alternative mechanisms are not necessarily exclusive in any particular situation, and all have been seen to apply in different model systems.
神经移植能够逆转许多与脑损伤相关的功能缺陷,无论这些脑损伤是由创伤、毒素、神经退行性变还是基因因素引起的。在一些模型系统中,恢复可以是部分的或完全的;而在其他系统中,移植的效果有限,甚至可能实际上导致进一步的功能障碍。为了制定合理有效的移植策略,有必要了解移植发挥功能作用的机制。已经提出了几种可能的机制,包括手术的非特异性后果、急性弥漫性神经营养和生长机制、慢性弥漫性释放缺乏的神经化学物质、为宿主再生提供桥接组织、对宿主脑进行弥漫性再支配,以及移植体与宿主的相互重新连接。这些机制在任何特定情况下不一定相互排斥,并且在不同的模型系统中都有应用。