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丙戊酸钠低剂量改善睡眠剥夺引起的感觉运动门控缺陷。

Sodium valproate improves sensorimotor gating deficit induced by sleep deprivation at low doses.

机构信息

Applied Psychology Master’s Program, Institute of Health Sciences, Üsküdar University, İstanbul, Turkey

Department of Psychiatry, Faculty of Medicine, Üsküdar University, İstanbul, Turkey

出版信息

Turk J Med Sci. 2021 Jun 28;51(3):1521-1530. doi: 10.3906/sag-2011-229.

DOI:10.3906/sag-2011-229
PMID:33517611
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8283464/
Abstract

BACKGROUND/AIM: Sleep deprivation disrupts prepulse inhibition of acoustic startle reflex and can be used to mimic psychosis in ex- perimental animals. On the other hand, it is also a model for other disorders of sensory processing, including migraine. This study aims to assess the effects of sodium valproate, a drug that is used in a variety of neuropsychiatric disorders, on normal and disrupted sensorimotor gating in rats.

MATERIALS AND METHODS

Sixty-two Wistar albino rats were randomly distributed into 8 groups. Subchronic and intraperitoneal sodium valproate were administrated to the sleep-deprived and nonsleep-deprived rats by either 50–100 or 200 mg/kg/day. Prepulse inhibition test and locomotor activity test were performed. Sleep deprivation induced by the modified multiple platform method.

RESULTS

Sleep deprivation impaired prepulse inhibition, decreased startle amplitude, and increased locomotor activity. Sodium valpro- ate did not significantly alter prepulse inhibition and locomotor activity in nonsleep-deprived and sleep-deprived groups. On the other hand, all doses decreased locomotor activity in drug-treated groups, and low dose improved sensorimotor gating and startle amplitude after sleep deprivation.

CONCLUSION

Low-dose sodium valproate improves sleep deprivation-disrupted sensorimotor gating, and this finding may rationalize the use of sodium valproate in psychotic states and other sensory processing disorders. Dose-dependent effects of sodium valproate on sensorimotor gating should be investigated in detail.

摘要

背景/目的:睡眠剥夺会破坏声反射的前脉冲抑制,可用于模拟实验动物的精神病。另一方面,它也是其他感觉处理障碍的模型,包括偏头痛。本研究旨在评估丙戊酸钠(一种用于多种神经精神疾病的药物)对正常和睡眠剥夺大鼠感觉运动门控的影响。

材料和方法

62 只 Wistar 白化大鼠随机分为 8 组。亚慢性和腹腔内给予丙戊酸钠,睡眠剥夺和非睡眠剥夺大鼠分别给予 50-100 或 200mg/kg/天。进行前脉冲抑制测试和运动活动测试。采用改良的多平台法诱导睡眠剥夺。

结果

睡眠剥夺会损害前脉冲抑制,降低起始幅度,增加运动活动。丙戊酸钠对非睡眠剥夺和睡眠剥夺组的前脉冲抑制和运动活动均无显著影响。另一方面,所有剂量均降低了药物治疗组的运动活动,而低剂量可改善睡眠剥夺后的感觉运动门控和起始幅度。

结论

低剂量丙戊酸钠可改善睡眠剥夺引起的感觉运动门控障碍,这一发现可能为丙戊酸钠在精神病和其他感觉处理障碍中的应用提供了合理性。应详细研究丙戊酸钠对感觉运动门控的剂量依赖性影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/f9a2eac8f711/turkjmedsci-51-1520-fig009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/75b4a65e8f39/turkjmedsci-51-1520-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/0dfc4d71336a/turkjmedsci-51-1520-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/0839beee870d/turkjmedsci-51-1520-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/b046732f7579/turkjmedsci-51-1520-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/acbe0f39f9bf/turkjmedsci-51-1520-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/93e67038949f/turkjmedsci-51-1520-fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/93632c3d5f90/turkjmedsci-51-1520-fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/890b30fa31ea/turkjmedsci-51-1520-fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/f9a2eac8f711/turkjmedsci-51-1520-fig009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/75b4a65e8f39/turkjmedsci-51-1520-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/0dfc4d71336a/turkjmedsci-51-1520-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/0839beee870d/turkjmedsci-51-1520-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/b046732f7579/turkjmedsci-51-1520-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/acbe0f39f9bf/turkjmedsci-51-1520-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/93e67038949f/turkjmedsci-51-1520-fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/93632c3d5f90/turkjmedsci-51-1520-fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/890b30fa31ea/turkjmedsci-51-1520-fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3679/8283464/f9a2eac8f711/turkjmedsci-51-1520-fig009.jpg

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Current Status of Antiepileptic Drugs as Preventive Migraine Therapy.
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