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Imbalance in cerebral protein homeostasis: Effects on memory consolidation.
Behavioural Brain Research ( IF 2.6 ) Pub Date : 2020-06-11 , DOI: 10.1016/j.bbr.2020.112767
Roberto A Prado-Alcalá 1 , Sofía González-Salinas 1 , Anaid Antaramián 2 , Gina L Quirarte 1 , Paola C Bello-Medina 3 , Andrea C Medina 1
Affiliation  

The long-standing hypothesis that memory consolidation is dependent upon de novo protein synthesis is based primarily on the amnestic effects of systemic administration of protein synthesis inhibitors (PSIs). Early experiments on mice showed that PSIs produced interference with memory consolidation that was dependent on the doses of PSIs, on the interval between drug injection and training, and, importantly, on the degree and duration of protein synthesis inhibition in the brain. Surprisingly, there is a conspicuous lack of information regarding the relationship between the duration of protein synthesis inhibition produced by PSIs and memory consolidation in the rat, one of the species most widely used to study memory processes. We found that, in the male rat, a single injection of cycloheximide, a commonly used PSI, produced a significant imbalance in protein homeostasis: an early inhibition of protein synthesis that lasted for at least one hour, followed by hyperproduction of proteins that lasted three days. We evaluated memory consolidation of inhibitory avoidance trained with either low or high intensity of foot-shock at the peaks of protein synthesis inhibition and protein hyperproduction. We found that, independent of the moment of training, the low-foot-shock groups showed amnesia, while the high-foot-shock groups displayed optimal memory performance. These results indicate that memory consolidation of relatively weak training is impaired by the inhibition or hyperproduction of protein synthesis, and that intense training overcomes this dysregulation of protein homeostasis allowing for memory formation probably through non-genomic mechanisms.



中文翻译:

脑蛋白质稳态失衡:对记忆巩固的影响。

记忆巩固依赖于从头的长期假设蛋白质合成主要基于蛋白质合成抑制剂 (PSI) 全身给药的遗忘效应。早期的小鼠实验表明,PSI 对记忆巩固产生干扰,这取决于 PSI 的剂量、药物注射和训练之间的间隔,以及重要的是,取决于大脑中蛋白质合成抑制的程度和持续时间。令人惊讶的是,关于 PSI 产生的蛋白质合成抑制持续时间与大鼠记忆巩固之间关系的信息明显缺乏,大鼠是最广泛用于研究记忆过程的物种之一。我们发现,在雄性大鼠中,单次注射放线菌酮(一种常用的 PSI)会导致蛋白质稳态显着失衡:蛋白质合成的早期抑制持续了至少一小时,随后蛋白质的过度生产持续了三天。我们评估了在蛋白质合成抑制和蛋白质过度生产的高峰期用低强度或高强度足部休克训练的抑制性回避的记忆巩固。我们发现,与训练时间无关,低足电击组表现出健忘症,而高足电击组则表现出最佳的记忆力。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。随后是持续三天的蛋白质过度生产。我们评估了在蛋白质合成抑制和蛋白质过度生产的高峰期用低强度或高强度足部休克训练的抑制性回避的记忆巩固。我们发现,与训练时间无关,低足电击组表现出健忘症,而高足电击组则表现出最佳的记忆力。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。随后是持续三天的蛋白质过度生产。我们评估了在蛋白质合成抑制和蛋白质过度生产的高峰期用低强度或高强度足部休克训练的抑制性回避的记忆巩固。我们发现,与训练时间无关,低足电击组表现出健忘症,而高足电击组则表现出最佳的记忆力。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。我们评估了在蛋白质合成抑制和蛋白质过度生产的高峰期用低强度或高强度足部休克训练的抑制性回避的记忆巩固。我们发现,与训练时间无关,低足电击组表现出健忘症,而高足电击组则表现出最佳的记忆力。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。我们评估了在蛋白质合成抑制和蛋白质过度生产的高峰期用低强度或高强度足部休克训练的抑制性回避的记忆巩固。我们发现,与训练时间无关,低足电击组表现出健忘症,而高足电击组则表现出最佳的记忆力。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。而高足电击组则显示出最佳的记忆性能。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。而高足电击组则显示出最佳的记忆性能。这些结果表明,相对较弱训练的记忆巩固会因蛋白质合成的抑制或过度产生而受损,而高强度训练克服了蛋白质稳态失调,可能通过非基因组机制形成记忆。

更新日期:2020-07-08
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