Long-term potentiation in vivo increases rat hippocampal tenascin-C expression.

Long-term potentiation in vivo increases rat hippocampal tenascin-C expression.
复制标题

体内长时程增强可增加大鼠海马腱蛋白-C 的表达。

DOI:
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发表时间:
1998
期刊:
Journal of Neurobiology
影响因子:
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通讯作者:
Melitta Schachner
Melitta Schachner
中科院分区:
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文献类型:
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作者:
Marina Nakic;Denise Manahan;K. Reymann;Melitta Schachner

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我们研究了高频强直电刺激(HFT)诱导大鼠齿状回长时程增强(LTP)后细胞外基质糖蛋白Tenascin-C的表达。原位杂交和免疫细胞化学分别从mRNA和蛋白水平检测Tenascin-C的表达。对照组未检测到Tenascin-C基因的表达,HFT后4h齿状回颗粒细胞层中Tenascin-C基因表达水平升高。HFT后24 h,Tenascin-C mRNA已恢复到对照水平。高频照射后4h,Tenascin-C蛋白在CA1区的放射层、放射层、分子层及齿状回颗粒细胞层内的狭窄区域内均有表达。然而,在高频辐射后24小时,在齿状回的分子层观察到更多的Tenascin-C免疫反应斑块。未接受刺激、低频刺激或在N-甲基-D-天冬氨酸受体拮抗剂D(-)-2-氨基-5-膦戊酸或代谢性谷氨酸受体拮抗剂(R,S)-α-甲基-4-羧基苯甘氨酸存在的情况下,对照组动物的Tenascin基因或蛋白水平没有增加。这些观察结果暗示了Tenascin-C在N-甲基-D-天冬氨酸和代谢性谷氨酸受体依赖的变化中的作用,伴随着LTP的诱导和/或维持。
We investigated the expression of the extracellular matrix glycoprotein tenascin-C after induction of long-term potentiation (LTP) by high-frequency tetanization (HFT) in the rat dentate gyrus in vivo. Expression of tenascin-C was evaluated at the mRNA and protein levels by in situ hybridization and immunocytochemistry, respectively. Whereas no tenascin-C mRNA was detectable in control animals, an increase in tenascin-C mRNA levels was observed in the granule cell layer of the dentate gyrus 4 h after HFT. At 24 h after HFT, tenascin-C mRNA had returned to control levels. Expression of tenascin-C protein 4 h after HFT followed that of controls in that tenascin was detectable in the strata oriens and radiatum of CA1, in the molecular layer, and within a narrow area at the inner surface of the granule cell layer in the dentate gyrus. However, 24 h after HFT, additional patches of tenascin-C immunoreactivity were observed in the molecular layer of the dentate gyrus. No increase in tenascin mRNA or protein levels was detected in control animals that received no stimulation, low-frequency stimulation, or HFT in the presence of the N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid or the metabotropic glutamate receptor antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine. These observations implicate a role for tenascin-C in N-methyl-D-aspartate and metabotropic glutamate receptor-dependent changes accompanying induction and/or maintenance of LTP.
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