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低频刺激通过激活内源性大麻素系统预防点燃诱导的损伤。

Low-Frequency Stimulation Prevents Kindling-Induced Impairment through the Activation of the Endocannabinoid System.

机构信息

Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.

Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

出版信息

Biomed Res Int. 2021 Jun 16;2021:5526780. doi: 10.1155/2021/5526780. eCollection 2021.

DOI:10.1155/2021/5526780
PMID:34222471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8225428/
Abstract

BACKGROUND

Cannabinoid system affects memory and has anticonvulsant effects in epileptic models. In the current study, the role of cannabinoid 1 (CB1) receptors was investigated in amelioration of the effects of low-frequency stimulation (LFS) on learning and memory impairments in kindled rats.

METHODS

Electrical stimulation of the hippocampal CA1 area was employed to kindle the animals. LFS was applied to the CA1 area in four trials following the last kindling stimulation. One group of animals received intraperitoneal injection of AM251 (0.1 g/rat), a CB1 receptor antagonist, before the LFS application. Similarly, CB1 agonist WIN55-212-2 (WIN) was administrated to another group prior to LFS. The Morris water maze (MWM) and the novel object recognition (NOR) tests were executed 48 h after the last kindling stimulation to assess learning and memory.

RESULTS

Applying LFS in the kindled+LFS group restored learning and memory impairments in the kindled rats. There was a significant difference between the kindled and the kindled+LFS groups in learning and memory. The application of AM251 reduced the LFS effects significantly. Adversely, WIN acted similarly to LFS and alleviated learning and memory deficits in the kindled+WIN group. In addition, WIN did not counteract the LFS enhancing effects in the KLFS+WIN group.

CONCLUSIONS

Improving effects of LFS on learning and memory impairments are mediated through the activation of the endocannabinoid (ECB) system.

摘要

背景

大麻素系统会影响记忆，并在癫痫模型中具有抗惊厥作用。在目前的研究中，研究了大麻素 1 (CB1) 受体在改善低频刺激 (LFS) 对点燃大鼠学习和记忆障碍的影响中的作用。

方法

用电刺激海马 CA1 区来点燃动物。在最后一次点燃刺激后，进行四次 CA1 区 LFS 应用。一组动物在 LFS 应用前腹腔注射 AM251（0.1 g/rat），一种 CB1 受体拮抗剂。同样，在 LFS 之前，另一个组给予 CB1 激动剂 WIN55-212-2 (WIN)。在最后一次点燃刺激后 48 小时进行 Morris 水迷宫 (MWM) 和新物体识别 (NOR) 测试，以评估学习和记忆。

结果

在点燃+LFS 组中应用 LFS 恢复了点燃大鼠的学习和记忆障碍。在学习和记忆方面，点燃组和点燃+LFS 组之间存在显著差异。AM251 的应用显著降低了 LFS 的效果。相反，WIN 类似于 LFS，并减轻了点燃+WIN 组的学习和记忆缺陷。此外，WIN 没有抵消 KLFS+WIN 组中 LFS 的增强作用。

结论

LFS 对学习和记忆障碍的改善作用是通过激活内源性大麻素 (ECB) 系统介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/931f9117f03a/BMRI2021-5526780.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/bebde3204f24/BMRI2021-5526780.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/fd549921b78b/BMRI2021-5526780.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/55b9d237b9ba/BMRI2021-5526780.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/931f9117f03a/BMRI2021-5526780.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/bebde3204f24/BMRI2021-5526780.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/fd549921b78b/BMRI2021-5526780.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/55b9d237b9ba/BMRI2021-5526780.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e5/8225428/931f9117f03a/BMRI2021-5526780.004.jpg

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Low-Frequency Electrical Stimulation Reduces the Impairment in Synaptic Plasticity Following Epileptiform Activity in Rat Hippocampal Slices through α, But Not α, Adrenergic Receptors.低频电刺激通过α而非α肾上腺素能受体减少大鼠海马切片癫痫样活动后突触可塑性的损伤。
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The role of 5-HT receptors of hippocampal CA1 region in anticonvulsant effects of low-frequency stimulation in amygdala kindled rats.
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Physiol Behav. 2018 Nov 1;196:119-125. doi: 10.1016/j.physbeh.2018.08.025. Epub 2018 Sep 1.
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