Ahmad F J, Joshi H C, Centonze V E, Baas P W
Department of Anatomy, University of Wisconsin Medical School, Madison 53706.
Neuron. 1994 Feb;12(2):271-80. doi: 10.1016/0896-6273(94)90270-4.
We tested the dependence of axon growth on microtubule (MT) nucleation from the neuronal centrosome. Nocodazole diminished MTs in freshly plated neurons by > 99%. Within 5 min of drug removal, MTs reassembled at the centrosome. This response was inhibited in cells microinjected with gamma-tubulin antibody. Within 2 hr of drug removal, uninjected neurons grew > 500 microns of axon. In roughly half of the antibody-injected cells, axon growth was abolished and MT levels were reduced by approximately 87% compared with uninjected cells. In the other antibody-injected cells, axon growth was compromised but not abolished, and MT levels were reduced by approximately 38%. Thus inhibition of MT nucleation at the centrosome hindered MT reassembly, and depending on the severity of this response, axon growth was either compromised or abolished.
我们测试了轴突生长对源自神经元中心体的微管（MT）成核的依赖性。诺考达唑使刚接种的神经元中的微管减少了99%以上。在去除药物后的5分钟内，微管在中心体重新组装。这种反应在用γ-微管蛋白抗体显微注射的细胞中受到抑制。在去除药物后的2小时内，未注射的神经元长出了超过500微米的轴突。在大约一半注射了抗体的细胞中，轴突生长被消除，与未注射的细胞相比，微管水平降低了约87%。在其他注射了抗体的细胞中，轴突生长受到损害但未被消除，微管水平降低了约38%。因此，中心体处微管成核的抑制阻碍了微管的重新组装，并且根据这种反应的严重程度，轴突生长要么受到损害要么被消除。
