Department of Physiology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan.
J Appl Physiol (1985). 2010 Dec;109(6):1635-43. doi: 10.1152/japplphysiol.00515.2010. Epub 2010 Sep 16.
Exposure to a hypergravity environment induces acute transient hypophagia, which is partially restored by a vestibular lesion (VL), suggesting that the vestibular system is involved in the afferent pathway of hypergravity-induced hypophagia. When rats were placed in a 3-G environment for 14 days, Fos-containing cells increased in the paraventricular hypothalamic nucleus, the central nucleus of the amygdala, the medial vestibular nucleus, the raphe nucleus, the nucleus of the solitary tract, and the area postrema. The increase in Fos expression was completely abolished or significantly suppressed by VL. Therefore, these regions may be critical for the initiation and integration of hypophagia. Because the vestibular nucleus contains serotonergic neurons and because serotonin (5-HT) is a key neurotransmitter in hypophagia, with possible involvement in motion sickness, we hypothesized that central 5-HT increases during hypergravity and induces hypophagia. To examine this proposition, the 5-HT concentrations in the cerebrospinal fluid were measured when rats were reared in a 3-G environment for 14 days. The 5-HT concentrations increased in the hypergravity environment, and these increases were completely abolished in rats with VL. Furthermore, a 5-HT(2A) antagonist (ketanserin) significantly reduced 3-G (120 min) load-induced Fos expression in the medial vestibular nucleus, and chronically administered ketanserin ameliorated hypergravity-induced hypophagia. These results indicate that hypergravity induces an increase in central 5-HT via the vestibular input and that this increase plays a significant role in hypergravity-induced hypophagia. The 5-HT(2A) receptor is involved in the signal transduction of hypergravity stress in the vestibular nucleus.
暴露于超重力环境会引起急性短暂性食欲减退，而前庭病变 (VL) 可部分恢复这种食欲减退，这表明前庭系统参与了超重力引起的食欲减退的传入途径。当大鼠被置于 3-G 环境中 14 天时，含有 Fos 的细胞在室旁下丘脑核、杏仁核中央核、前庭内侧核、中缝核、孤束核和后极区增加。VL 完全消除或显著抑制 Fos 表达的增加。因此，这些区域可能对食欲减退的启动和整合至关重要。由于前庭核含有 5-羟色胺能神经元，而 5-羟色胺 (5-HT) 是食欲减退的关键神经递质，可能与运动病有关，我们假设在超重力下中枢 5-HT 增加并引起食欲减退。为了检验这一假设，当大鼠在 3-G 环境中饲养 14 天时，测量了脑脊液中的 5-HT 浓度。在超重力环境中，5-HT 浓度增加，而在具有 VL 的大鼠中，这些增加完全被消除。此外，5-HT2A 拮抗剂 (酮色林) 显著降低了 3-G(120min)负荷诱导的前庭内侧核中的 Fos 表达，而慢性给予酮色林改善了超重力引起的食欲减退。这些结果表明，超重力通过前庭输入引起中枢 5-HT 的增加，并且这种增加在超重力引起的食欲减退中起重要作用。5-HT2A 受体参与了前庭核中超重力应激的信号转导。
