Bone histomorphometric and biomechanical abnormalities in mice homozygous for deletion of the dopamine transporter gene
Bone histomorphometric and biomechanical abnormalities in mice homozygous for deletion of the dopamine transporter gene
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DOI：
10.1016/s8756-3282(99)00232-x
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发表时间：
2000-01-01
期刊：
影响因子：
4.1
通讯作者：
Caron, MG
中科院分区：
文献类型：
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作者：
Bliziotes, M;McLoughlin, S;Caron, MG
据报道，多巴胺（DA）对钙和磷代谢有影响。多巴胺转运体（DAT）被认为通过快速摄取神经递质进入突触前末端来控制释放的多巴胺的时间和空间活动。我们已经评估了DA转运基因（DAT）缺失的小鼠骨骼的组织学和生物力学特性，以帮助描述DA在骨骼生物学中的作用。我们已经证明DAT（-/-）小鼠骨量和强度降低。DAT（-/-）动物股骨长度和干重较短。DAT（-/-）小鼠股骨灰质钙含量比野生型小鼠低32%。DAT（-/-）组动物胫骨近端干骺端松质骨体积显著降低（p < 0.04）。对于椎骨，由于小梁间距增加（p < 0.05）和小梁数量减少（p < 0.05）， DAT（-/-）动物的松质骨体积再次低于野生型（p = NS）。DAT（-/-）组小鼠股骨骨干皮质厚度和骨面积均减少。DAT（-/-）小鼠的极限弯曲负荷（股强度）比野生型小鼠低30% （p = 0.004）。因此，DAT基因的缺失会导致骨骼结构和完整性的缺陷。(C) 2000年由爱思唯尔科学公司版权所有。
Dopamine (DA) has been reported to have effects on calcium and phosphorus metabolism. The dopamine transporter (DAT) is believed to control the temporal and spatial activity of released DA by rapid uptake of the neurotransmitter into presynaptic terminals. We have evaluated the histologic and biomechanical properties of the skeleton in mice homozygous for deletion of the DA transporter gene (DAT) to help delineate the role of DA in bone biology. We have demonstrated that DAT(-/-) mice have reduced bone mass and strength. DAT(-/-) animals had shorter femur length and dry weight. Ash calcium content of the femur was 32% lower in the DAT(-/-) mice than in the wild-type animals. Cancellous bone volume in the proximal tibial metaphysis was significantly lower in the DAT(-/-) animals (p, < 0.04). There was a 32% reduction in trabecular thickness (p = NS), For the vertebrae, cancellous bone volume was again lower in the DAT(-/-) animals compared with wild-type as a consequence of increased trabecular spacing (p < 0.05) and reduced trabecular number (p < 0.05). Cortical thickness and bone area in the femoral diaphysis were reduced in the DAT(-/-) animals. The ultimate bending load (femoral strength) for the DAT(-/-) mice was 30% lower than the wild-type mice (p = 0.004). Thus, deletion of the DAT gene results in deficiencies in skeletal structure and integrity. (C) 2000 by Elsevier Science Inc. All rights reserved.