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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient hippocampus
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Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient hippocampus

机译：脑源性神经营养因子可恢复多唾液酸-神经细胞粘附分子缺陷型海马的长期增强作用

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摘要

The neural cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) contribute to long-term potentiation (LTP) in the CA1 hippocampus. Here we report that the deficient LTP found in slices prepared from NCAM knockout mice and in organotypic slice cultures treated with Endo-N. an enzyme that cleaves the PSA moiety of NCAM, can be rescued by brain-derived neurotrophic factor (BDNF). This effect is not reproduced by nerve growth factor, but can be obtained with high concentrations of NT4/5. The effect of BDNF cannot be accounted for by modifications of Nmethyl-D- aspartate receptor-dependent responses or of high-frequency bursts. PSA-NCAM, however, could directly interact with BDNF. Exogenous application of PSA residues or recombinant PSA-NCAM also prevents LTP. Furthermore trkB phosphorylation. and thus BDNF signaling. is reduced in both NCAM knockout mice and Endo-N-treated slice cultures. These results suggest that one action of PSA-NCAM could be to sensitize pyramidal neurons to BDNF. thereby modulating activity-dependent synaptic plasticity.
机译：神经细胞粘附分子（NCAM）及其多唾液酸化形式（PSA-NCAM）有助于CA1海马体的长期增强（LTP）。在这里，我们报道在从NCAM基因敲除小鼠制备的切片和用Endo-N处理的器官型切片培养物中发现的LTP不足。可以通过脑源性神经营养因子（BDNF）挽救可切割NCAM PSA部分的酶。神经生长因子不能重现这种作用，但高浓度的NT4 / 5可获得。 BDNF的影响不能通过修饰N甲基-D-天冬氨酸受体依赖性反应或高频猝发来解释。但是，PSA-NCAM可以直接与BDNF相互作用。 PSA残基或重组PSA-NCAM的外源应用也可以防止LTP。此外，trkB磷酸化。因此，BDNF信号传导。在NCAM基因敲除小鼠和Endo-N处理的切片培养物中均降低。这些结果表明，PSA-NCAM的作用之一可能是使锥体神经元对BDNF敏感。从而调节活动依赖的突触可塑性。

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