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Br-16a does not interfere with alpha - 2 noradrenergic and dopamine postsynaptic receptor functioning.BR-16a 不会干扰α-2 去甲肾上腺素能和多巴胺突触后受体的功能。
Indian J Psychiatry. 1993 Jul;35(3):179-80.
2
Herbal pharmacotherapy for the attenuation of electroconvulsive shock-induced anterograde and retrograde amnestic deficits.用于减轻电休克诱发的顺行性和逆行性记忆缺失的草药药物治疗。
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BR-16A protects against ECS-induced anterograde amnesia.BR-16A可预防内源性大麻素系统(ECS)诱导的顺行性遗忘。
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ECT-induced anterograde amnesia: can the deficits be minimized?电休克治疗所致顺行性遗忘:能否将缺陷最小化?
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Evidence for nootropic effect of BR-16A (Mentat), a herbal psychotropic preparation, in mice.草本精神药物制剂BR-16A(门塔特)对小鼠促智作用的证据。
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High but not low ECS stimulus intensity augments apomorphine-stimulated dopamine postsynaptic receptor functioning in rats.高而非低的内源性大麻素系统(ECS)刺激强度可增强阿扑吗啡刺激的大鼠多巴胺突触后受体功能。
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The alpha 2-adrenoceptor antagonist atipamezole potentiates anti-Parkinsonian effects and can reduce the adverse cardiovascular effects of dopaminergic drugs in rats.α2肾上腺素能受体拮抗剂阿替美唑可增强抗帕金森病作用,并能减轻多巴胺能药物对大鼠的不良心血管影响。
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Neurochemical regulation of feeding in the rat: facilitation by alpha-noradrenergic, but not dopaminergic, receptor stimulants.大鼠进食的神经化学调节:α-去甲肾上腺素能受体激动剂可促进进食,而多巴胺能受体激动剂则不能。
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Molecular biology research in neuropsychiatry: India's contribution.神经精神医学分子生物学研究:印度的贡献。
Indian J Psychiatry. 2010 Jan;52(Suppl 1):S120-7. doi: 10.4103/0019-5545.69223.
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Molecular mechanisms underlying electroconvulsive therapy-induced amnestic deficits: A decade of research.电休克治疗所致记忆缺陷的分子机制:十年研究
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本文引用的文献

1
Effect of a herbal psychotropic preparation, BR-16A (Mentat), on performance of mice on elevated plus-maze.一种草本精神药物制剂BR-16A(门塔特)对小鼠在高架十字迷宫实验中行为表现的影响。
Indian J Exp Biol. 1991 Dec;29(12):1120-3.
2
Evidence for nootropic effect of BR-16A (Mentat), a herbal psychotropic preparation, in mice.草本精神药物制剂BR-16A(门塔特)对小鼠促智作用的证据。
Indian J Physiol Pharmacol. 1992 Jan;36(1):29-34.
3
Prevention of development of tolerance and dependence to opiate in mice by BR-16A (Mentat), a herbal psychotropic preparation.草本精神药物制剂BR-16A(门塔特)对小鼠阿片类药物耐受性和依赖性形成的预防作用
Indian J Exp Biol. 1992 Oct;30(10):885-8.

BR-16a 不会干扰α-2 去甲肾上腺素能和多巴胺突触后受体的功能。

Br-16a does not interfere with alpha - 2 noradrenergic and dopamine postsynaptic receptor functioning.

机构信息

Chiitaranjan Andrade, MD, Associate Professor, Department of Psychopharmacology, NIMHANS, Bangalore - 560 029.

出版信息

Indian J Psychiatry. 1993 Jul;35(3):179-80.

PMID:21743635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2978492/
Abstract

BR-16A is a herbal preparation with several putative psychotropic effects. Recent work has suggested that it facilities certain aspects of cognition and that it ameliorates ECT-induced amnesia in animal models. The present study sought to assess whether it affects noradrenergic and dopaminergic functioning in the central nervous system. Adult male Sprague-Dawley rats received BR-16A (200mg/kg) or vehicle for one month. The animals were subsequently challenged with clonidine (100 mg/kg I.P.), apomorphine (2mg/kg I.P.), or saline in a factorial design, and motility of the animals was immediately thereafter assessed using a small open field. BR-16A neither attenuated clonidine induced alpha-2 noradrenergic receptor-mediated hypomotility nor accentuated apomorphine-induced dopamine postsynaptic receptor-mediated hypermotility, suggesting that it does not interfere with alpha-2 noradrenergic and dopamine postsynaptic receptor functioning.

摘要

BR-16A 是一种具有多种潜在精神活性作用的草药制剂。最近的研究表明,它有助于认知的某些方面,并改善动物模型中的电休克诱导的健忘症。本研究旨在评估它是否影响中枢神经系统中的去甲肾上腺素能和多巴胺能功能。成年雄性 Sprague-Dawley 大鼠接受 BR-16A(200mg/kg)或载体治疗一个月。随后,动物在因子设计中接受可乐定(100mg/kg IP)、阿扑吗啡(2mg/kg IP)或生理盐水的挑战,并且动物的运动性立即使用小的开放场进行评估。BR-16A 既没有减弱可乐定诱导的α-2 去甲肾上腺素能受体介导的低运动性,也没有加重阿扑吗啡诱导的多巴胺突触后受体介导的高运动性,表明它不干扰α-2 去甲肾上腺素能和多巴胺突触后受体的功能。