Wecker L, Marrero-Rosado B, Engberg M E, Johns B E, Philpot R M
Department of Psychiatry and Behavioral Neurosciences, University of South Florida Morsani College of Medicine, Tampa, FL, United States.
Department of Psychiatry and Behavioral Neurosciences, University of South Florida Morsani College of Medicine, Tampa, FL, United States.
Neurotoxicology. 2017 Jan;58:143-152. doi: 10.1016/j.neuro.2016.11.010. Epub 2016 Dec 13.
3-acetylpyridine (3-AP) is a metabolic antagonist used in research to decrease levels of nicotinamide (niacinamide) in laboratory animals. The administration of 3-AP followed by nicotinamide to rats leads to the selective destruction of neurons in the medial inferior olive, resulting in a loss of climbing fibers innervating cerebellar Purkinje cells and a consequent ataxia manifest by alterations in both balance and gait. Although 3-AP has also been administered to mice to destroy neurons in the inferior olive, there are limited studies quantifying the consequent effects on balance, and no studies on gait. Further, the relationship between 3-AP-induced lesions of the inferior olive and behavior has not been elucidated. Because 3-AP continues to be used for experiments involving mice, this study characterized the effects of this toxin on both balance and gait, and on the neuronal integrity of several brain regions involved in motor coordination. Results indicate that C57BL/6 mice are less sensitive to the neurotoxic effects of 3-AP than rats, and a dose more than 6.5 times that used for rats produces deficits in both balance and gait comparable to those in rats. This dose led to a significant (p<0.05) loss of NeuN(+) neurons in several subregions of the inferior olive including the rostral medial nucleus, dorsomedial cell column, ventrolateral protrusion, and cap of Kooy. Further, the number of NeuN(+) neurons in these subregions, with the exception of the dorsomedial cell column, was significantly (p<0.05) related to rotorod performance, implicating their involvement in this behavior.
3-乙酰吡啶(3-AP)是一种代谢拮抗剂,用于研究中降低实验动物体内烟酰胺(尼克酰胺)的水平。给大鼠先注射3-AP再注射烟酰胺会导致内侧下橄榄核中的神经元选择性破坏,从而导致支配小脑浦肯野细胞的攀缘纤维丧失,进而出现平衡和步态改变所表现出的共济失调。尽管也给小鼠注射过3-AP以破坏下橄榄核中的神经元,但定量评估其对平衡影响的研究有限,且尚无关于步态的研究。此外,3-AP诱导的下橄榄核损伤与行为之间的关系尚未阐明。由于3-AP仍用于涉及小鼠的实验,本研究对这种毒素对平衡和步态以及对参与运动协调的几个脑区神经元完整性的影响进行了表征。结果表明,C57BL/6小鼠对3-AP的神经毒性作用比大鼠更不敏感,给予大鼠剂量6.5倍以上的剂量会导致与大鼠相当的平衡和步态缺陷。该剂量导致下橄榄核几个亚区(包括吻侧内侧核、背内侧细胞柱、腹外侧突出部和库伊帽)中NeuN(+)神经元显著(p<0.05)减少。此外,除背内侧细胞柱外,这些亚区中NeuN(+)神经元的数量与转棒试验表现显著(p<0.05)相关,表明它们参与了这种行为。