Francisco Elian da Silva, Mendes-da-Silva Rosângela Figueiredo, de Castro Cássia Borges Lima, Soares Geórgia de Sousa Ferreira, Guedes Rubem Carlos Araújo
Departamento de Nutrição, Universidade Federal de Pernambuco, Recife, Brazil.
Departamento de Educação Física, Centro Universitário Católico de Quixadá, Quixadá, Brazil.
Front Neurosci. 2019 Sep 18;13:981. doi: 10.3389/fnins.2019.00981. eCollection 2019.
This study aimed to evaluate the possible protective role of taurine on anxiety-like behavior, brain electrical activity and glial cell immunoreactivity in well-nourished and malnourished rats that were treated with a subconvulsing dose of pilocarpine. Newborn Wistar rats were subjected to normal or unfavorable lactation conditions, represented by the suckling of litters with 9 or 15 pups, resulting in well-nourished and malnourished animals, respectively. Each nutritional group was split into five subgroups that were treated from postnatal day (PND) 35 to 55 with 300 mg/kg/day of taurine + 45 mg/kg/day of pilocarpine (group T + P), taurine only (group T), pilocarpine only (group P), vehicle control (group V), or not treated control (group naïve; Nv). At PND56-58, the groups were subjected to the elevated plus-maze behavioral tests. Glycemia was measured on PND59. Between PND60 and PND65, the cortical spreading depression (CSD) was recorded in the cerebral cortex, and the levels of malondialdehyde and microglial and astrocyte immunoreactivity were evaluated in the cortex and hippocampus. Our data indicate that treatment with taurine and pilocarpine resulted in anxiolytic-like and anxiogenic behavior, respectively, and that nutritional deficiency modulated these effects. Both treatments decelerated CSD propagation and modulated GFAP- and Iba1-containing glial cells. Pilocarpine reduced body weight and glycemia, and administration of taurine was not able to attenuate the effects of pilocarpine. The molecular mechanisms underlying taurine action on behavioral and electrophysiological parameters in the normal and altered brain remain to be further explored.
本研究旨在评估牛磺酸对用亚惊厥剂量毛果芸香碱处理的营养良好和营养不良大鼠的焦虑样行为、脑电活动和胶质细胞免疫反应性的可能保护作用。新生Wistar大鼠分别处于正常或不利的哺乳条件下，即分别哺乳9只或15只幼崽的窝仔，从而分别产生营养良好和营养不良的动物。每个营养组又分为五个亚组，从出生后第35天（PND）至55天，分别用300mg/kg/天的牛磺酸 + 45mg/kg/天的毛果芸香碱处理（T + P组）、仅用牛磺酸处理（T组）、仅用毛果芸香碱处理（P组）、溶剂对照（V组）或未处理对照（未处理组；Nv）。在PND56 - 58时，对各组进行高架十字迷宫行为测试。在PND59时测量血糖。在PND60至PND65之间，记录大脑皮层的皮层扩散性抑制（CSD），并评估皮层和海马中丙二醛水平以及小胶质细胞和星形胶质细胞的免疫反应性。我们的数据表明，牛磺酸和毛果芸香碱处理分别导致抗焦虑样和致焦虑行为，并且营养缺乏调节了这些作用。两种处理均减缓了CSD的传播并调节了含GFAP和Iba1的胶质细胞。毛果芸香碱降低了体重和血糖，而给予牛磺酸并不能减轻毛果芸香碱的作用。牛磺酸对正常和改变的大脑中行为和电生理参数作用的分子机制仍有待进一步探索。
