Calretinin expression as a critical component in the control of dentate gyrus long-term potentiation induction in mice
Calretinin expression as a critical component in the control of dentate gyrus long-term potentiation induction in mice
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DOI：
10.1111/j.1460-9568.1998.00373.x
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发表时间：
1998-09-01
影响因子：
3.4
通讯作者：
Schurmans, S
中科院分区：
文献类型：
--
作者：
Gurden, H;Schiffmann, SN;Schurmans, S
我们最近报道，calretinin基因零突变的小鼠纯合（Cr-/-）损害了齿状回的长期增强（LTP）诱导(S, Schurmans et al. (1997) Proc. Natl。学会科学。在这里，我们研究了齿状LTP在小鼠杂合（Cr+/-）中对相同突变的诱导。尽管这些小鼠的神经元中存在calretinin，尽管与正常小鼠相比，calretinin的水平有所降低，但齿状回的LTP诱导完全受损。与Cr+/-小鼠一样，Cr+/-小鼠的空间记忆和学习能力未受影响。总之，我们的研究结果表明，calretinin是控制小鼠齿状突触可塑性的关键成分，并且需要高于Cr+/-小鼠的calretinin水平来诱导该区域的LTP。讨论了导致基因剂量与生物效应不相关的可能机制。
We have recently reported that mice homozygous (Cr-/-) for a null mutation in the calretinin gene have impaired long-term potentiation (LTP) induction in the dentate gyrus (S, Schurmans et al. (1997) Proc. Natl. Acad. Sci. USA, 94, 10415), Here, we investigated dentate LTP induction in mice heterozygous (Cr+/-) for the same mutation. Despite the presence of calretinin in neurons of these mice, although at reduced levels as compared with normal mice, LTP induction in dentate gyrus was totally impaired. Spatial memory and learning were found unaffected in Cr+/- mice, such as in Cr-/- mice. Altogether, our results suggest that calretinin is a critical component in the control of dentate synaptic plasticity in mice, and that levels of calretinin higher than those observed in Cr+/- mice are required to induce LTP in this area. The possible mechanisms leading to the absence of correlation between gene dosage and biological effects are discussed.