Sant'Ana Débora de Mello Gonçales, Gois Marcelo Biondaro, Hermes-Uliana Catchia, Pereira-Severi Letícia Sarturi, Baptista Emily Martins, Mantovani Luana Colognese, da Silva Aristeu Vieira, de Almeida Araújo Eduardo José
State University of Maringá, Department of Biosciences and Physiopathology, Maringá, PR, Brazil.
Federal University of Reconcavo of Bahia, Santo Antonio de Jesus, BA, Brazil.
Acta Histochem. 2017 May;119(4):423-427. doi: 10.1016/j.acthis.2017.04.008. Epub 2017 May 4.
In the enteric nervous system (ENS), nitrergic neurons produce and use nitric oxide (NO) as an inhibitory motor neurotransmitter in response to parasitic infections, including those caused by Toxoplasma gondii. However, damage to the host caused by NO has been reported by various authors, and the role of NO in protection or cytotoxicity continues to be extensively studied. In this study, nitrergic neurons were investigated in the myenteric plexus of the jejunum and the distal colon of rats infected with 500 oocysts of the M7741 strain of T. gondii. Ten rats were randomly assigned into a control group (CG) and infected group (IG; received 500 sporulated oocysts of T. gondii orally). After 24h, the rats were euthanized, and samples of the jejunum and distal colon were obtained and processed for NADPH-diaphorase histochemical analysis. Quantitative and morphometric analysis of the nitrergic neurons in whole mounts containing the myenteric plexus was performed. There was a numeric reduction of nitrergic neurons per mm in both jejunum and distal colon. The remaining nitrergic neurons suffered atrophy in the areas of the cell body and nucleus, which resulted in a decrease in cytoplasm. Thus, we conclude that an avirulent strain of T. gondii in a short time causes neuroplastic changes in the small and large intestine of rats.
在肠神经系统(ENS)中,含氮能神经元在应对包括由刚地弓形虫引起的寄生虫感染时,会产生并利用一氧化氮(NO)作为一种抑制性运动神经递质。然而,已有多位作者报道了NO对宿主造成的损害,并且NO在保护作用或细胞毒性方面的作用仍在被广泛研究。在本研究中,对感染了500个刚地弓形虫M7741株卵囊的大鼠空肠和远端结肠的肌间神经丛中的含氮能神经元进行了研究。将10只大鼠随机分为对照组(CG)和感染组(IG;经口接受500个刚地弓形虫孢子化卵囊)。24小时后,对大鼠实施安乐死,并获取空肠和远端结肠的样本,进行NADPH-黄递酶组织化学分析。对包含肌间神经丛的整装标本中的含氮能神经元进行了定量和形态计量分析。空肠和远端结肠中每毫米含氮能神经元的数量均减少。剩余的含氮能神经元在细胞体和细胞核区域出现萎缩,导致细胞质减少。因此,我们得出结论,无毒力的刚地弓形虫菌株在短时间内会引起大鼠小肠和大肠的神经可塑性变化。