Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion
Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion
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DOI：
10.1016/s0306-4522(02)00182-3
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发表时间：
2002-01-01
期刊：
影响因子：
3.3
通讯作者：
Sugimoto, T
中科院分区：
文献类型：
--
作者：
Ichikawa, H;Yamaai, T;Sugimoto, T
在Brn-3a野生型和敲除型小鼠胚胎第18.5天和出生后第0天的三叉神经节和口面组织中进行小白蛋白、钙结合蛋白D-28k、钙降钙素和降钙素基因相关肽（CGRP）的免疫组化。野生型小鼠三叉神经节中含有丰富的小白蛋白。calbindin D-28k和cgrp免疫反应神经元，而神经节中几乎没有calbindin免疫反应神经元。在Brn-3a敲除小鼠中，检测到小蛋白免疫反应神经元减少63%。相比之下，Brn-3a缺失显著增加calbindin d -28k免疫反应神经元数量（增加3.5倍）和calbindin免疫反应神经元数量（增加91倍）。然而，Brn-3a缺乏并没有改变cgrp免疫反应神经元的数量。细胞大小分析表明，Brn-3a的缺失增加了小（< 100 μm(2)）小白蛋白-、calbindin D-28k-和cgrp免疫反应神经元的比例，而减少了大（> 200 μm(2)）免疫反应细胞的比例。突变小鼠calretinin免疫反应神经元为小或中等（100-200 mum(2)）。在野生型小鼠的口腔-面部组织中含有细小蛋白、钙结合蛋白D-28k和cgrp免疫反应纤维，但没有钙结合蛋白免疫反应纤维。Brn-3a基因敲除小鼠眶下神经中细小蛋白免疫反应纤维数量明显减少，触须中细小蛋白免疫反应末梢消失。眼眶下神经和心神经中calbindin d -28k免疫反应纤维的数量明显增加。此外，在触须中出现calbindin d -28k免疫反应性末梢。在突变体的眶下神经中，一些纤维也表现出calretinin免疫反应性。而敲除小鼠的口面区cgrp免疫反应纤维未见明显变化。综上所述，我们的数据表明Brn-3a缺乏对三叉神经节中神经化学物质的表达有影响。(c) 2002年ibro。Elsevier Science Ltd.出版。版权所有。
Immunohistochemistry for parvalbumin, calbindin D-28k, calretinin and calcitonin gene-related peptide (CGRP) was performed on the trigeminal ganglion and oro-facial tissues in Brn-3a wildtype and knockout mice at embryonic day 18.5 and postnatal day 0. In wildtype mice, the trigeminal ganglion contained abundant parvalbumin-. calbindin D-28k- and CGRP-immunoreactive neurons while the ganglion was almost devoid of calretinin-immunoreactive neurons. In Brn-3a knockout mice, a 63% decrease of parvalbumin-immunoreactive neurons was detected. In contrast, the absence of Brn-3a dramatically increased the number of calbindin D-28k-immunoreactive (3.5-fold increase) and calretinin-immunoreactive neurons (91-fold increase). The number of CGRP-immunoreactive neurons, however, was not altered by the Brn-3a deficiency. Cell size analysis indicated that loss of Brn-3a increased the proportions of small ( < 100 μm(2)) parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while it decreased those of large (> 200 mum(2)) immunoreactive cells. Calretinin-immunoreactive neurons were either small or medium (100-200 mum(2)) in mutant mice. The oro-facial tissues contained parvalbumin, calbindin D-28k- and CGRP-immunoreactive fibers, but not calretinin-immunoreactive ones in wildtype mice. In Brn-3a knockout mice, the number of parvalbumin-immunoreactive fibers markedly decreased in the infraorbital nerve and parvalbumin-immunoreactive endings disappeared in the vibrissa. In contrast, the number of calbindin D-28k-immunoreactive fibers increased significantly in the infraorbital and mental nerves. In addition, calbindin D-28k-immunoreactive endings appeared in the vibrissa. As well, some fibers showed calretinin-immunoreactivity in the infraorbital nerve of the mutant. However, no obvious change of CGRP-immunoreactive fibers was observed in the oro-facial region of knockout mice.Taken together, our data suggest that Brn-3a deficiency has effects on the expression of neurochemical substances in the trigeminal ganglion. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.