Laboratório de Bioenergética, Programa de Pós-graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Behav Brain Res. 2012 May 16;231(1):92-6. doi: 10.1016/j.bbr.2012.03.004. Epub 2012 Mar 13.
Maple syrup urine disease (MSUD) is an autosomal recessive metabolic disorder resulting from deficiency of branched-chain α-keto acid dehydrogenase complex leading to branched chain amino acids (BCAA) leucine, isoleucine, and valine accumulation as well as their corresponding transaminated branched-chain α-keto acids. MSUD patients present neurological dysfunction and cognitive impairment. Here, we investigated whether acute and chronic administration of a BCAA pool causes impairment of acquisition and retention of avoidance memory in young rats. We have used two administration protocols. Acute administration consisted of three subcutaneous administrations of the BCAA pool (15.8 μL/g body weight at 1-h intervals) containing 190 mmol/L leucine, 59 mmol/L isoleucine, and 69 mmol/L valine or saline solution (0.85% NaCl; control group) in 30 days old Wistar rats. Chronic administration consisted of two subcutaneous administrations of BCAA pool for 21 days in 7 days old Wistar rats. N-acetylcysteine (NAC; 20 mg/kg) and deferoxamine (DFX; 20 mg/kg) co administration influence on behavioral parameters after chronic BCAA administration was also investigated. BCAA administration induced long-term memory impairment in the inhibitory avoidance and CMIA (continuous multiple-trials step-down inhibitory avoidance) tasks whereas with no alterations in CMIA retention memory. Inhibitory avoidance alterations were prevented by NAC and DFX. BCAA administration did not impair the neuropsychiatric state, muscle tone and strength, and autonomous function evaluated with the SHIRPA (SmithKline/Harwell/ImperialCollege/RoyalHospital/Phenotype Assessment) protocol. Taken together, our results indicate that alterations of motor activity or emotionality probably did not contribute to memory impairment after BCAA administration and NAC and DFX effects suggest that cognition impairment after BCAA administration may be caused by oxidative brain damage.
枫糖尿症(MSUD)是一种常染色体隐性遗传代谢疾病,由支链α-酮酸脱氢酶复合物缺陷引起,导致支链氨基酸(BCAA)亮氨酸、异亮氨酸和缬氨酸积累以及相应的转氨基支链α-酮酸。MSUD 患者表现出神经功能障碍和认知障碍。在这里,我们研究了急性和慢性给予支链氨基酸池是否会导致年轻大鼠获得和保留回避记忆的能力受损。我们使用了两种给药方案。急性给药包括在 30 天大的 Wistar 大鼠中进行三次皮下支链氨基酸池(每隔 1 小时给予 15.8 μL/g 体重,含 190 mmol/L 亮氨酸、59 mmol/L 异亮氨酸和 69 mmol/L 缬氨酸或生理盐水(0.85%NaCl;对照组)。慢性给药包括在 7 天大的 Wistar 大鼠中进行两次皮下支链氨基酸池给药,共 21 天。还研究了 N-乙酰半胱氨酸(NAC;20mg/kg)和去铁胺(DFX;20mg/kg)联合给药对慢性支链氨基酸给药后行为参数的影响。支链氨基酸给药导致抑制性回避和 CMIA(连续多次试验下抑制性回避)任务中的长期记忆障碍,而对 CMIA 保留记忆没有改变。NAC 和 DFX 可预防抑制性回避改变。支链氨基酸给药不会损害神经精神状态、肌肉张力和力量以及使用 SHIRPA(SmithKline/Harwell/ImperialCollege/RoyalHospital/PhenotypeAssessment)方案评估的自主功能。综上所述,我们的结果表明,运动活动或情绪改变可能不会导致支链氨基酸给药后的记忆障碍,而 NAC 和 DFX 的作用表明,支链氨基酸给药后的认知障碍可能是由氧化脑损伤引起的。