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外侧隔核刺激联合水迷宫训练可恢复齿状回长时程增强及改善空间学习记忆。

Basolateral amygdala stimulation plus water maze training restore dentate gyrus LTP and improve spatial learning and memory.

机构信息

Centro Internacional for Restauration Neurologica (CIREN), La Habana 11300, Cuba.

Universidad del Sinú "Elías Bechara Zainum", Montería, Colombia.

出版信息

Behav Brain Res. 2022 Jan 24;417:113589. doi: 10.1016/j.bbr.2021.113589. Epub 2021 Sep 20.

DOI:10.1016/j.bbr.2021.113589
PMID:34547342
Abstract

Synaptic plasticity is a key mechanism of neural plasticity involved in learning and memory. A reduced or impaired synaptic plasticity could lead to a deficient learning and memory. On the other hand, besides reducing hipocampal dependent learning and memory, fimbria-fornix lesion affects LTP. However, we have consistently shown that stimulation of the basolateral amygdala (BLA) 15 min after water maze training is able to improve spatial learning and memory in fimbria fornix lesioned rats while also inducing changes in the expression of plasticity-related genes expression in memory associated brain regions like the hippocampus and prefrontal cortex. In this study we test that hypothesis: whether BLA stimulation 15 min after water maze training can improve LTP in the hippocampus of fimbria-fornix lesioned rats. To address this question, we trained fimbria-fornix lesioned rats in water maze for four consecutive days, and the BLA was bilaterally stimulated 15 min after each training session.Our data show that trained fimbria-fornix lesioned rats develop a partially improved LTP in dentated gyrus compared with the non-trained fimbria-fornix lesioned rats. In contrast, dentated gyrus LTP in trained and BLA stimulated fimbria-fornix lesioned rats improved significantly compared to the trained fimbria-fornix lesioned rats, but was not different from that shown by healthy animals. BLA stimulation in non-trained FF lesioned rats did not improve LTP; instead produces a transient synaptic depression. Restoration of the ability to develop LTP by the combination of training and BLA stimulation would be one of the mechanisms involved in ameliorating memory deficits in lesioned animals.

摘要

突触可塑性是参与学习和记忆的神经可塑性的关键机制。突触可塑性降低或受损可能导致学习和记忆能力不足。另一方面,除了减少海马依赖性学习和记忆外,穹窿-海马伞损伤还会影响 LTP。然而,我们已经一致表明,在水迷宫训练后 15 分钟刺激外侧杏仁核(BLA)能够改善穹窿-海马伞损伤大鼠的空间学习和记忆,同时还会诱导与记忆相关的大脑区域(如海马体和前额叶皮层)中与可塑性相关的基因表达的变化。在这项研究中,我们检验了这样一个假设:水迷宫训练后 15 分钟 BLA 刺激是否可以改善穹窿-海马伞损伤大鼠的海马体 LTP。为了解决这个问题,我们在水迷宫中对穹窿-海马伞损伤大鼠进行了连续四天的训练,并且在每次训练后 15 分钟对双侧 BLA 进行刺激。我们的数据显示,与未经训练的穹窿-海马伞损伤大鼠相比,经过训练的穹窿-海马伞损伤大鼠在齿状回中产生了部分改善的 LTP。相比之下,在经过训练和 BLA 刺激的穹窿-海马伞损伤大鼠中,齿状回 LTP 显著改善,与健康动物相似。在未经训练的 FF 损伤大鼠中,BLA 刺激不能改善 LTP;反而会产生短暂的突触抑制。通过训练和 BLA 刺激的结合来恢复产生 LTP 的能力可能是改善损伤动物记忆缺陷的机制之一。

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