Greferath U, Mallard C, Roufail E, Rees S M, Barrett G L, Bartlett P F
Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3010, Australia.
Neurosci Lett. 2002 Oct 25;332(1):57-60. doi: 10.1016/s0304-3940(02)00928-x.
The induction of the p75 neurotrophin receptor (p75NTR) on striatal cholinergic neurons by global hypoxic-ischemia has been reported to promote neuron survival. We have found, however, while the p75NTR-expressing neurons survive the insult for the first 5 days, subsequently they undergo shrinkage, loss of choline acetyl transferase (ChAT) expression, and more than 96% are eventually lost by 8 days. In contrast ChAT-expressing cells in the surrounding region of the infarction, do not express p75NTR and there is no evidence of neuronal loss. These results suggest the expression of p75NTR on cholinergic interneurons of the rat striatum is associated with delayed neuronal degeneration.
据报道,全脑缺氧缺血可诱导纹状体胆碱能神经元上的p75神经营养因子受体(p75NTR)表达,从而促进神经元存活。然而,我们发现,虽然表达p75NTR的神经元在损伤后的前5天能够存活,但随后它们会发生萎缩,胆碱乙酰转移酶(ChAT)表达丧失,到第8天时,超过96%的此类神经元最终会死亡。相比之下,梗死灶周边区域表达ChAT的细胞不表达p75NTR,且没有神经元丢失的迹象。这些结果表明,大鼠纹状体胆碱能中间神经元上p75NTR的表达与神经元的延迟变性有关。