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本体感觉传入神经在TrkC基因敲除小鼠的咬肌中存活。

Proprioceptive afferents survive in the masseter muscle of trkC knockout mice.

作者信息

Matsuo S, Ichikawa H, Silos-Santiago I, Arends J J, Henderson T A, Kiyomiya K, Kurebe M, Jacquin M F

机构信息

Department of Toxicology, School of Veterinary Medicine, Osaka Prefecture University, Sakai, Japan.

出版信息

Neuroscience. 2000;95(1):209-16. doi: 10.1016/s0306-4522(99)00424-8.

Abstract

Peripheral innervation patterns of proprioceptive afferents from dorsal root ganglia and the mesencephalic trigeminal nucleus were assessed in trkC-deficient mice using immunohistochemistry for protein gene product 9.5 and parvalbumin. In trkC knockout mice, spinal proprioceptive afferents were completely absent in the limb skeletal muscles, M. biceps femoris and M. gastrocnemius, as previously reported. In these same animals, however, proprioceptive afferents from mesencephalic trigeminal nucleus innervated masseter muscles and formed primary endings of muscle spindles. Three wild-type mice averaged 35.7 spindle profiles (range: 31-41), six heterozygotes averaged 32.3 spindles (range: 27-41), and four homozygotes averaged 32.8 spindles (range: 26-42). Parvalbumin and Nissl staining of the brain stem showed approximately 50% surviving mesencephalic trigeminal sensory neurons in trkC-deficient mice. TrkC-/- mice (n = 5) had 309.4 +/- 15.9 mesencephalic trigeminal sensory cells versus 616.5 +/- 26.3 the sensory cells in trkC+/+ mice (n = 4). These data indicate that while mesencephalic trigeminal sensory neurons are significantly reduced in number by trkC deletion, they are not completely absent. Furthermore, unlike their spinal counterparts, trigeminal proprioceptive afferents survive and give rise to stretch receptor complexes in masseter muscles of trkC knockout mice. This indicates that spinal and mesencephalic trigeminal proprioceptive afferents have different neurotrophin-supporting system during survival and differentiation. It is likely that one or more other neurotrophin receptors expressed in mesencephalic trigeminal proprioceptive neurons of trkC knockout mice compensate for the lack of normal neurotrophin-3 signaling through trkC.

摘要

利用蛋白质基因产物9.5和小白蛋白的免疫组织化学方法,在TrkC基因缺陷小鼠中评估了来自背根神经节和中脑三叉神经核的本体感觉传入神经的外周神经支配模式。如先前报道,在TrkC基因敲除小鼠中,肢体骨骼肌、股二头肌和腓肠肌中完全没有脊髓本体感觉传入神经。然而,在这些相同的动物中,来自中脑三叉神经核的本体感觉传入神经支配咬肌并形成肌梭的初级末梢。三只野生型小鼠平均有35.7个肌梭轮廓(范围:31 - 41),六只杂合子平均有32.3个肌梭(范围:27 - 41),四只纯合子平均有32.8个肌梭(范围:26 - 42)。脑干的小白蛋白和尼氏染色显示,在TrkC基因缺陷小鼠中约50%的中脑三叉神经感觉神经元存活。TrkC -/- 小鼠(n = 5)有309.4 ± 15.9个中脑三叉神经感觉细胞,而TrkC +/+ 小鼠(n = 4)有616.5 ± 26.3个感觉细胞。这些数据表明,虽然中脑三叉神经感觉神经元的数量因TrkC缺失而显著减少,但它们并未完全缺失。此外,与脊髓中的对应神经不同,三叉神经本体感觉传入神经存活下来,并在TrkC基因敲除小鼠的咬肌中形成牵张感受器复合体。这表明脊髓和中脑三叉神经本体感觉传入神经在存活和分化过程中有不同的神经营养因子支持系统。很可能在TrkC基因敲除小鼠的中脑三叉神经本体感觉神经元中表达的一种或多种其他神经营养因子受体补偿了通过TrkC正常神经营养因子-3信号的缺乏。

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