Lourenssen S, Roder J C, Blennerhassett M G
Gastrointestinal Diseases Research Unit, Queen's University, Hotel Dieu Hospital, 166 Brock Street, Kingston, Ontario, Canada.
Neurosci Lett. 2000 Mar 3;281(1):25-8. doi: 10.1016/s0304-3940(00)00809-0.
Over-activation of glutamate receptors is implicated in neurodegeneration. Using mice with a deletion in the GluR2 gene, we studied the sensitivity of sympathetic neurons to reduced levels of nerve growth factor (NGF), which can cause neuronal cell death. Under standard culture conditions of 50 ng/ml NGF, neurons from the superior cervical ganglion survived and grew equally well compared with wild type controls. However, the subsequent reduction of NGF levels caused significantly poorer survival among mutant neurons by 48 h, at 44+/-13% of control at 10 ng/ml NGF, and dropping further to 14+/-6% at 0.05 ng/ml NGF. These results suggest that the absence of GluR2 impairs the ability of these NGF-sensitive neurons to survive under limiting amounts of this neurotrophic factor.
谷氨酸受体的过度激活与神经退行性变有关。我们利用GluR2基因缺失的小鼠，研究了交感神经元对神经生长因子（NGF）水平降低的敏感性，NGF水平降低可导致神经元细胞死亡。在50 ng/ml NGF的标准培养条件下，与野生型对照相比，颈上神经节的神经元存活并生长良好。然而，随后NGF水平的降低导致突变神经元在48小时后的存活率显著降低，在10 ng/ml NGF时为对照的44±13%，在0.05 ng/ml NGF时进一步降至14±6%。这些结果表明，GluR2的缺失损害了这些对NGF敏感的神经元在这种神经营养因子有限量情况下的存活能力。
