1型肌醇1,4,5-三磷酸受体是小脑浦肯野神经元中长时程抑制诱导所必需的。
Type 1 inositol 1,4,5-trisphosphate receptor is required for induction of long-term depression in cerebellar Purkinje neurons.
作者信息
Inoue T, Kato K, Kohda K, Mikoshiba K
机构信息
Department of Molecular Neurobiology, The Institute of Medical Science, The University of Tokyo, Tokyo-108, Japan.
出版信息
J Neurosci. 1998 Jul 15;18(14):5366-73. doi: 10.1523/JNEUROSCI.18-14-05366.1998.
Abstract
The inositol 1,4,5-trisphosphate receptor (InsP3R) is an intracellular Ca2+ channel that releases Ca2+ from internal Ca2+ stores in response to InsP3. Although InsP3R is highly expressed in various regions of the mammalian brain, the functional role of this receptor has not been clarified. We show here that cerebellar slices prepared from mice with a disrupted InsP3R type 1 gene, which is predominantly expressed in Purkinje cells, completely lack long-term depression (LTD), a model of synaptic plasticity in the cerebellum. Moreover, a specific antibody against InsP3R1, introduced into wild-type Purkinje cells through patch pipettes, blocked the induction of LTD. These data indicate that, in addition to Ca2+ influx through Ca2+ channels on the plasma membrane, Ca2+ release from InsP3R plays an essential role in the induction of LTD, suggesting a physiological importance for InsP3R in Purkinje cells.
摘要
肌醇1,4,5 -三磷酸受体（InsP3R）是一种细胞内Ca2+通道，可响应InsP3从细胞内Ca2+储存库释放Ca2+。尽管InsP3R在哺乳动物大脑的各个区域高度表达，但该受体的功能作用尚未阐明。我们在此表明，从1型InsP3R基因敲除小鼠制备的小脑切片完全缺乏长时程抑制（LTD），LTD是小脑突触可塑性的一种模型，而1型InsP3R基因主要在浦肯野细胞中表达。此外，通过膜片吸管将针对InsP3R1的特异性抗体引入野生型浦肯野细胞，可阻断LTD的诱导。这些数据表明，除了通过质膜上的Ca2+通道流入Ca2+外，InsP3R释放Ca2+在LTD的诱导中起重要作用，提示InsP3R在浦肯野细胞中具有生理重要性。
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