Chapter 4 Cell death in models of spinal cord injury

摘要: Current treatments for acute spinal cord injury are based on animal models of human (SCI). These have shown that the initial traumatic to tissue is followed by a long period secondary includes number cellular and biochemical cascades. processes potential targets therapies. Continued refinement rat mouse SCI, along with more detailed analyses biology lesion in these models, points both necrotic apoptotic mechanisms cell death after SCI. In this chapter, we review recent evidence long-term oligodendrocytes tracts undergoing Wallerian degeneration following This process appears be related closely activation microglial cells. It has been thought cells might source cytotoxic cytokines, such as tumor necrosis factor-alpha (TNF-alpha), kill oligodendrocytes. However, vivo suggests TNF-alpha itself may not induce or apoptosis We data other possible pathways apoptosis, neurotrophin receptor p75 which expressed neurons SCI rats mice. addition, it important Ninety minutes moderate contusion lesion, microglia activated surround dying neurons. an 'atraumatic' model now greatly potentiate mediated glutamate receptors. studies emphasize multiple interactions contribute study new approaches studying will needed maximize strategies chronic therapies, neural repair.