Kawano Akiyo, Honma Shiho, Inui-Yamamoto Chizuko, Ito Akira, Niwa Hitoshi, Wakisaka Satoshi
Department of Oral Anatomy and Developmental Biology, Osaka University Graduate School of Dentistry, Japan; Department of Dental Anesthesiology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Department of Oral Anatomy and Developmental Biology, Osaka University Graduate School of Dentistry, Japan.
Brain Res. 2017 Mar 15;1659:1-7. doi: 10.1016/j.brainres.2017.01.020. Epub 2017 Jan 19.
Zinc deficiency causes various symptoms including taste disorders. In the present study, changes in expression of c-Fos immunoreactivity in neurons of the parabrachial nucleus (PBN), one of the relay nuclei for transmission of gustatory information, after bitter stimulation to the dorsal surface of the tongue were examined in zinc-deficient rats. Experimental zinc-deficient animals were created by feeding a low-zinc diet for 4weeks, and showed the following symptoms of zinc deficiency: low body weight, low serum zinc content and behavioral changes to avoid bitter stimulation. In normal control animals, intraoral application of 1mM quinine caused increased numbers of c-Fos-immunoreactive (c-Fos-IR) neurons in the external lateral subnucleus and external medial subnucleus of the PBN (elPBN and emPBN, respectively) compared with application of distilled water. However, in the zinc-deficient animals, the numbers of c-Fos-IR neurons in the elPBN and emPBN did not differ significantly between application of quinine and distilled water. After feeding the zinc-deficient animals a normal diet for 4weeks, the symptoms of zinc deficiency recovered, and the expression of c-Fos-IR neurons following intraoral bitter stimulation became identical to that in the normal control animals. The present results indicate that dietary zinc deficiency causes alterations to neuronal activities in the gustatory neural circuit, and that these neuronal alterations can be reversed by changing to a normal diet.
锌缺乏会导致包括味觉障碍在内的各种症状。在本研究中，对缺锌大鼠在舌背进行苦味刺激后，检查了臂旁核（PBN）神经元中c-Fos免疫反应性的表达变化，PBN是味觉信息传递的中继核之一。通过喂食低锌饮食4周来建立实验性缺锌动物模型，这些动物表现出以下缺锌症状：体重减轻、血清锌含量降低以及避免苦味刺激的行为变化。在正常对照动物中，与应用蒸馏水相比，口腔内应用1mM奎宁会导致PBN的外侧外核和内侧外核（分别为elPBN和emPBN）中c-Fos免疫反应性（c-Fos-IR）神经元数量增加。然而，在缺锌动物中，应用奎宁和蒸馏水后，elPBN和emPBN中c-Fos-IR神经元的数量没有显著差异。给缺锌动物喂食正常饮食4周后，缺锌症状恢复，口腔内苦味刺激后c-Fos-IR神经元的表达与正常对照动物相同。目前的结果表明，饮食锌缺乏会导致味觉神经回路中的神经元活动发生改变，并且通过改为正常饮食可以逆转这些神经元改变。
