Trichothecene mycotoxins, a family of common contaminants on cereal grains, are known to negatively impact human and animal health with adverse effect on food consumption being of particular concern. T-2 toxin has been previously demonstrated to induce anorectic response in several animal species including mouse, rat, rabbit. Although the T-2 toxin-induced anorectic response has been associated with the release of gut satiety hormone, much less is known about the role of neurotransmitter in this response. To address this gap, we employed a nocturnal mouse food refusal model to test the hypothesis that neurotransmitters 5-hydroxytryptamine (5-HT) and substance P (SP) mediate anorexia induction by T-2 toxin. Elevations of plasma 5-HT and SP markedly corresponded to anorexia induction following oral exposure to T-2 toxin. Direct administration of exogenous 5-HT and SP induced anorectic responses similar to T-2 toxin. The 5-HT3 receptor (5-HT3R) antagonist granisetron evoked a dose-dependent attenuation of both 5-HT- and T-2 toxin-induced anorectic responses. Pretreatment with neurokinin-1 receptor (NK-1R) antagonist Emend^® dose-dependently attenuated both SP- and T-2 toxin-induced anorectic responses. To summarize, the results suggest that both 5-HT and SP play important roles in anorexia induction by T-2 toxin. 5-HT is more potent and long-acting than SP in this response.

已知曲霉烯霉菌毒素是谷物上的一种常见污染物，对人类和动物健康产生负面影响，对食品消费的负面影响尤为令人关注。先前已证明T-2毒素可在几种动物物种（包括小鼠，大鼠，兔子）中引起厌食反应。尽管T-2毒素诱导的厌食反应与肠道饱腹感激素的释放有关，但对神经递质在该反应中的作用了解甚少。为了解决这一差距，我们采用了夜间小鼠拒食模型来测试神经递质5-羟色胺（5-HT）和P物质（SP）介导T-2毒素引起厌食的假设。口服T-2毒素后血浆5-HT和SP升高明显对应于厌食诱导。直接施用外源5-HT和SP会引起类似于T-2毒素的厌食反应。5-HT3受体（5-HT3R）拮抗剂Granisetron引起5-HT-和T-2毒素诱导的厌食反应的剂量依赖性减弱。神经激肽1受体（NK-1R）拮抗剂Emend预处理^®剂量依赖性地减弱了SP和T-2毒素引起的厌食反应。总之，结果表明5-HT和SP在T-2毒素引起的厌食症中均起重要作用。在此反应中，5-HT比SP更有效和更长效。