Calefi Atilio Sersun, Fonseca Juliana Garcia da Silva, Nunes Catarina Augusta de Queiroz, Lima Ana Paula Nascimento, Quinteiro-Filho Wanderley Moreno, Flório Jorge Camilo, Zager Adriano, Ferreira Antonio José Piantino, Palermo-Neto João
Department of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Av. Prof. Dr. Orlando Marques de Paiva, 87, São Paulo 05508-900, Brazil.
Vet Sci. 2019 Jan 9;6(1):4. doi: 10.3390/vetsci6010004.
Heat stress has been related to the impairment of behavioral and immunological parameters in broiler chickens. However, the literature is not clear on the involvement of neuroimmune interactions in a heat stress situation associated with bacterial and parasitic infections. The present study evaluated the production of monoamines and their metabolites in brain regions (rostral pallium, hypothalamus, brain stem, and midbrain) in broiler chickens submitted to chronic heat stress and/or infection and co-infection with spp. and type A. The heat stress and avian necrotic enteritis (NE) modulated the neurochemical profile of monoamines in different areas of the central nervous system, in particular, those related to the activity of the hypothalamus-hypophysis-adrenal (HPA) axis that is responsible for sickness behavior. and/or infection, heat stress increased 5-hydroxytryptamine (5-HT), 4,4 dihydroxyphenylacetic acid (DOPAC), and DOPAC/dopamine (DA) in the rostral pallium; 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), homovanillic acid (HVA), HVA/DA, DOPAC/DA, and 5-hydroxyindoleacetic acid (5-HIAA)/5-HT in the hypothalamus; MHPG, 5-HIAA/5-HT, DOPAC/DA, and HVA/DA in the midbrain; and MHPG, DOPAC, HVA, HVA/DA, DOPAC/DA, and 5-HIAA/5-HT in the brainstem. Heat stress decreased noradrenaline + norepinephrine (NOR + AD) in all brain regions analyzed; 5-HT in the hypothalamus, midbrain, and brainstem; and DA in the midbrain. The results also showed the existence and activity of the brain-gut axis in broiler chickens. The brain neurochemical profile and corticosterone production are consistent with those observed in chronic stressed mammals, in animals with sickness behavior, and an overloading of the HPA axis.
热应激与肉鸡行为和免疫参数的损害有关。然而,关于神经免疫相互作用在与细菌和寄生虫感染相关的热应激情况下的参与情况,文献并不明确。本研究评估了遭受慢性热应激和/或感染以及与 spp. 和 A 型共同感染的肉鸡脑区(吻侧皮层、下丘脑、脑干和中脑)中单胺及其代谢产物的产生。热应激和禽坏死性肠炎(NE)调节了中枢神经系统不同区域中单胺的神经化学特征,特别是那些与负责疾病行为的下丘脑 - 垂体 - 肾上腺(HPA)轴活动相关的区域。和/或感染时,热应激会增加吻侧皮层中的 5 - 羟色胺(5 - HT)、4,4 - 二羟基苯乙酸(DOPAC)以及 DOPAC/多巴胺(DA);增加下丘脑中的 3 - 甲氧基 - 4 - 羟基苯乙二醇(MHPG)、高香草酸(HVA)、HVA/DA、DOPAC/DA 以及 5 - 羟吲哚乙酸(5 - HIAA)/5 - HT;增加中脑中的 MHPG、5 - HIAA/5 - HT、DOPAC/DA 以及 HVA/DA;增加脑干中的 MHPG、DOPAC、HVA、HVA/DA、DOPAC/DA 以及 5 - HIAA/5 - HT。热应激会降低所有分析脑区中的去甲肾上腺素 + 去甲肾上腺素(NOR + AD);降低下丘脑、中脑和脑干中的 5 - HT;降低中脑中的 DA。结果还显示了肉鸡中脑肠轴的存在和活性。脑神经化学特征和皮质酮的产生与在慢性应激哺乳动物、有疾病行为的动物以及 HPA 轴过载的动物中观察到的情况一致。