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首页> 外文期刊>Neurochemical Research >Self-Stimulation Rewarding Experience Restores Stress-Induced CA3 Dendritic Atrophy, Spatial Memory Deficits and Alterations in the Levels of Neurotransmitters in the Hippocampus
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Self-Stimulation Rewarding Experience Restores Stress-Induced CA3 Dendritic Atrophy, Spatial Memory Deficits and Alterations in the Levels of Neurotransmitters in the Hippocampus

机译:自我刺激的奖励经验可恢复应激诱导的CA3树突萎缩,空间记忆障碍和海马神经递质水平的改变

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Chronic restraint stress causes spatial learning and memory deficits, dendritic atrophy of the hippocampal pyramidal neurons and alterations in the levels of neurotransmitters in the hippocampus. In contrast, intracranial self-stimulation (ICSS) rewarding behavioral experience is known to increase dendritic arborization, spine and synaptic density, and increase neurotransmitter levels in the hippocampus. In addition, ICSS facilitates operant and spatial learning, and ameliorates fornix-lesion induced behavioral deficits. Although the effects of stress and ICSS are documented, it is not known whether ICSS following stress would ameliorate the stress-induced deficits. Accordingly, the present study was aimed to evaluate the role of ICSS on stress-induced changes in hippocampal morphology, neurochemistry, and behavioral performance in the T-maze. Experiments were conducted on adult male Wistar rats, which were randomly divided into four groups; normal control, stress (ST), self-stimulation (SS), and stress + self-stimulation (ST + SS). Stress group of rats were subjected to restraint stress for 6 h daily over 21 days, SS group animals were subjected to SS from ventral tegmental area for 10 days and ST + SS rats were subjected to restraint stress for 21 days followed by 10 days of SS. Interestingly, our results show that stress-induced behavioral deficits, dendritic atrophy, and decreased levels of neurotransmitters were completely reversed following 10 days of SS experience. We propose that SS rewarding behavioral experience ameliorates the stress-induced cognitive deficits by inducing structural and biochemical changes in the hippocampus.
机译:慢性束缚应激导致空间学习和记忆缺陷,海马锥体神经元树突萎缩以及海马神经递质水平的改变。相反,已知颅内自刺激(ICSS)奖励行为经验会增加树突状树突,脊柱和突触密度,并增加海马中的神经递质水平。另外,ICCSS促进了操作和空间学习,并减轻了穹隆病变引起的行为缺陷。尽管已经记录了压力和ICSS的影响,但尚不清楚压力后ICSS是否会减轻由压力引起的缺陷。因此,本研究旨在评估ICSS在应激诱导的T型迷宫海马形态,神经化学和行为表现变化中的作用。对成年雄性Wistar大鼠进行实验,将其随机分为四组。正常控制,压力(ST),自我刺激(SS)和压力+自我刺激(ST + SS)。应激组的大鼠在21天内每天承受束缚压力6小时,SS组的动物从腹侧被盖区受到SS承受10天,而ST + SS大鼠的束缚应力承受21天,然后承受SS的持续10天。有趣的是,我们的结果显示,在SS经历10天后,压力引起的行为缺陷,树突萎缩和神经递质水平下降被完全逆转。我们建议SS奖励的行为经验通过诱导海马结构和生化变化来缓解应激诱导的认知缺陷。

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