Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Brazil. aleksandro
Vet Parasitol. 2011 Feb 10;175(3-4):237-44. doi: 10.1016/j.vetpar.2010.10.021. Epub 2010 Oct 20.
Neurological and locomotor clinical signs are described in animals infected with Trypanosoma evansi. These disturbances may be related to changes in the amount of acetylcholine (neurotransmitter) in the synaptic cleft. Therefore, changes in acetylcholinesterase (AChE) activity and lipid peroxidation in brain and spinal cord of T. evansi-infected rats were investigated. Each rat was intraperitoneally infected with 10(6) trypomastigotes kept in fresh (group A; n=13) and cryopreserved blood (group B; n=13). Thirteen served as uninfected (not-infected; group C). In days 4 and 30 post-infection (PI) the rats were anesthetized and subsequently decapitated to obtain the brain and the spinal cord (between vertebrae L1 and S2). The brain was removed and dissected (cerebellum, cerebral cortex, striatum and hippocampus) to measure the activity of AChE and lipid peroxidation, determined by TBARS levels. To verify if T. evansi was present in the central nervous system (CNS), brain structures of three rats of each group were processed by PCR T. evansi-specific. AChE activity was significantly increased in all brain structures and decrease in spinal cord in infected rats in 4 PI (P<0.05). The levels of TBARS were decreased in the brain structures, differently from spinal cord, which showed increased lipid peroxidation in 4 PI. The AChE activity in striatum, cerebral cortex, hippocampus and spinal cord reduced concomitantly with the increase of the enzyme in cerebellum of the infected rats (P<0.05), and the TBARS levels increased in cerebellum, striatum and spinal cord of infected rats compared to non-infected animals in 30 PI. The PCR was positive for T. evansi in all structures of the brain, confirming the presence of the parasite in the CNS. Based on the results, we conclude that the changes in AChE activity and lipid peroxidation in the CNS are induced by infection with T. evansi, suggesting that the parasite interferes with the cholinergic neurotransmission in this experimental condition.
感染伊氏锥虫（Trypanosoma evansi）的动物会出现神经和运动临床症状。这些紊乱可能与突触间隙中乙酰胆碱（神经递质）的量有关。因此，研究了伊氏锥虫感染大鼠的脑和脊髓中的乙酰胆碱酯酶（AChE）活性和脂质过氧化变化。每只大鼠经腹腔感染新鲜（A 组，n=13）和冷冻保存（B 组，n=13）的 10（6）个锥虫。13 只为未感染（C 组）。感染后第 4 和 30 天（PI）麻醉大鼠并断头取脑和脊髓（L1 和 S2 之间）。取出大脑并解剖（小脑、大脑皮层、纹状体和海马）以测量 AChE 活性和脂质过氧化，通过 TBARS 水平确定。为了验证伊氏锥虫是否存在于中枢神经系统（CNS）中，每组 3 只大鼠的脑结构进行了 T. evansi 特异性 PCR。在感染大鼠中，在第 4 PI 时所有脑结构中的 AChE 活性均显著升高，而脊髓中的 AChE 活性降低（P<0.05）。在脑结构中，TBARS 水平降低，而在脊髓中，脂质过氧化在第 4 PI 时增加。感染大鼠的纹状体、大脑皮层、海马和脊髓中的 AChE 活性与小脑中的酶活性同时降低（P<0.05），并且在第 30 PI 时，感染大鼠的小脑、纹状体和脊髓中的 TBARS 水平与未感染动物相比增加。PCR 对所有脑结构均为 T. evansi 阳性，证实寄生虫存在于 CNS 中。基于这些结果，我们得出结论，CNS 中 AChE 活性和脂质过氧化的变化是由 T. evansi 感染引起的，这表明寄生虫在这种实验条件下干扰了胆碱能神经传递。
