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转圈小鼠海马中海钙结合蛋白 D28-k、钙结合蛋白 Parvalbumin 和钙网蛋白的分布变化。

Changes in the distribution of calbindin D28-k, parvalbumin, and calretinin in the hippocampus of the circling mouse.

机构信息

Department of Anatomy, Institute of Medical Center, Dankook University, San#29, Anseo-dong, Cheonan-si, Chungnam 330-714, South Korea.

出版信息

Brain Res. 2012 Feb 9;1437:58-68. doi: 10.1016/j.brainres.2011.12.009. Epub 2011 Dec 13.

DOI:10.1016/j.brainres.2011.12.009
PMID:22226504
Abstract

The circling (cir) mouse strain, a murine model of deafness caused by a spontaneous mutation, exhibits characteristic behaviors of circling and hyperactivity. In an induced-noise paradigm, cir mice display a significant loss in their spatial orientation abilities, and this has been suggested to be due at least in part to changes in calcium homeostasis. Auditory information is transferred from the cochlear nucleus to the hippocampus, where it is processed to modulate motor and sensory activity. Such a pathway could be affected at the cellular level by alterations in neurotransmission, including alterations that involve Ca(2+). However, there have been no studies in a hearing deficit model examining the concomitant molecular alterations in the hippocampus. Thus, in the present study we used immunohistochemistry to compare the distribution of the calcium-binding proteins (CaBPs) calbindin D-28k, parvalbumin, and calretinin in the hippocampi of heterozygous (+/cir), homozygous (cir/cir), and wild-type (+/+) mice. The expression of the CaBPs in various hippocampal subfields appeared to be significantly lower in cir mice (+/- and -/-) than in +/+ mice. Such a decrease in CaBP expression in cir/cir mice would alter calcium homeostasis, which in turn could affect the connection of the tri-synaptic circuit of the hippocampus as well as the cortical region. A decrease in CaBPs and the probable resultant glutamate-mediated excitability could contribute to the functional changes that lead to the characteristic behavioral features of cir mice.

摘要

Circling(cir)小鼠品系是一种自发性突变导致耳聋的小鼠模型,表现出典型的转圈和过度活跃行为。在诱发噪声范式中,cir 小鼠表现出空间定向能力的显著丧失,这至少部分归因于钙稳态的变化。听觉信息从耳蜗核传递到海马体,在那里进行处理以调节运动和感觉活动。这种途径可能会在细胞水平上受到神经传递的改变的影响,包括涉及 Ca(2+)的改变。然而,在听力缺陷模型中,尚未有研究检查海马体中同时发生的分子改变。因此,在本研究中,我们使用免疫组织化学比较了钙结合蛋白(CaBPs)钙结合蛋白 D-28k、副甲状腺蛋白和钙调蛋白在杂合子(+/cir)、纯合子(cir/cir)和野生型(+/+)小鼠海马体中的分布。在 cir 小鼠(+/ 和 -/-)中,各种海马体亚区的 CaBP 表达似乎明显低于+/+小鼠。cir/cir 小鼠中 CaBP 表达的这种减少会改变钙稳态,进而可能影响海马体的三突触回路以及皮质区域的连接。CaBPs 的减少和可能由此产生的谷氨酸能兴奋性可能有助于导致 cir 小鼠特征性行为特征的功能变化。

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