Pickering Mark, Cumiskey Derval, O'Connor John J
Department of Human Anatomy and Physiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Exp Physiol. 2005 Sep;90(5):663-70. doi: 10.1113/expphysiol.2005.030734. Epub 2005 Jun 8.
Increasing attention is being paid to the role of inflammatory and immune molecules in the modulation of central nervous system (CNS) function. Tumour necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine, the receptors for which are expressed on neurones and glial cells throughout the CNS. Through the action of its two receptors, it has a broad range of actions on neurones which may be either neuroprotective or neurotoxic. It plays a facilitatory role in glutamate excitotoxicity, both directly and indirectly by inhibiting glial glutamate transporters on astrocytes. Additionally, TNF-alpha has direct effects on glutamate transmission, for example increasing expression of AMPA receptors on synapses. TNF-alpha also plays a role in synaptic plasticity, inhibiting long-term potentiation (LTP), a process dependent on p38 mitogen activated kinase (p38 MAP) kinase. In the following review we look at these and other effects of TNF-alpha in the CNS.
炎症和免疫分子在调节中枢神经系统（CNS）功能中的作用正受到越来越多的关注。肿瘤坏死因子-α（TNF-α）是一种促炎细胞因子，其受体在整个中枢神经系统的神经元和胶质细胞上均有表达。通过其两种受体的作用，它对神经元具有广泛的作用，这些作用可能具有神经保护作用或神经毒性。它在谷氨酸兴奋性毒性中发挥促进作用，直接或间接通过抑制星形胶质细胞上的胶质谷氨酸转运体来实现。此外，TNF-α对谷氨酸传递有直接影响，例如增加突触上AMPA受体的表达。TNF-α还在突触可塑性中发挥作用，抑制长时程增强（LTP），这一过程依赖于p38丝裂原活化蛋白激酶（p38 MAP）。在以下综述中，我们将探讨TNF-α在中枢神经系统中的这些及其他作用。
