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贯叶金丝桃素通过激活 Ca(2+) 通透性 TRPC6 通道调节海马锥体神经元树突棘形态。

Hyperforin modulates dendritic spine morphology in hippocampal pyramidal neurons by activating Ca(2+) -permeable TRPC6 channels.

机构信息

Department of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.

出版信息

Hippocampus. 2013 Jan;23(1):40-52. doi: 10.1002/hipo.22052. Epub 2012 Jul 20.

Abstract

The standardized extract of the St. John's wort plant (Hypericum perforatum) is commonly used to treat mild to moderate depression. Its active constituent is hyperforin, a phloroglucinol derivative that reduces the reuptake of serotonin and norepinephrine by increasing intracellular Na(+) concentration through the activation of nonselective cationic TRPC6 channels. TRPC6 channels are also Ca(2+) -permeable, resulting in intracellular Ca(2+) elevations. Indeed, hyperforin activates TRPC6-mediated currents and Ca(2+) transients in rat PC12 cells, which induce their differentiation, mimicking the neurotrophic effect of nerve growth factor. Here, we show that hyperforin modulates dendritic spine morphology in CA1 and CA3 pyramidal neurons of hippocampal slice cultures through the activation of TRPC6 channels. Hyperforin also evoked intracellular Ca(2+) transients and depolarizing inward currents sensitive to the TRPC channel blocker La(3+) , thus resembling the actions of the neurotrophin brain-derived neurotrophic factor (BDNF) in hippocampal pyramidal neurons. These results suggest that the antidepressant actions of St. John's wort are mediated by a mechanism similar to that engaged by BDNF.

摘要

贯叶金丝桃的标准化提取物(贯叶连翘)通常用于治疗轻度至中度抑郁症。其有效成分是金丝桃素,是一种邻苯三酚葡萄糖衍生物,通过激活非选择性阳离子 TRPC6 通道增加细胞内 Na+浓度,从而减少 5-羟色胺和去甲肾上腺素的再摄取。TRPC6 通道也是 Ca2+ 可渗透的,导致细胞内 Ca2+ 升高。事实上,金丝桃素激活大鼠 PC12 细胞中的 TRPC6 介导的电流和 Ca2+ 瞬变,诱导其分化,模拟神经营养因子神经生长因子的神经保护作用。在这里,我们表明金丝桃素通过激活 TRPC6 通道调节海马切片培养物 CA1 和 CA3 锥体神经元的树突棘形态。金丝桃素还引起细胞内 Ca2+ 瞬变和去极化内向电流,对 TRPC 通道阻滞剂 La3+ 敏感,因此类似于神经营养因子脑源性神经营养因子 (BDNF) 在海马锥体神经元中的作用。这些结果表明贯叶金丝桃的抗抑郁作用是通过类似于 BDNF 参与的机制介导的。

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本文引用的文献

1
Dendritic spines, synaptic plasticity and neuronal survival: activity shapes dendritic spines to enhance neuronal viability.
Eur J Neurosci. 2010 Jun;31(12):2178-84. doi: 10.1111/j.1460-9568.2010.07270.x. Epub 2010 Jun 9.
2
Chronic fluoxetine treatment induces structural plasticity and selective changes in glutamate receptor subunits in the rat cerebral cortex.
Neuroscience. 2010 Aug 11;169(1):98-108. doi: 10.1016/j.neuroscience.2010.04.035. Epub 2010 Apr 22.
3
The spine apparatus, synaptopodin, and dendritic spine plasticity.
Neuroscientist. 2010 Apr;16(2):125-31. doi: 10.1177/1073858409355829.
5
6
Synaptic adaptations of CA1 pyramidal neurons induced by a highly effective combinational antidepressant therapy.
Biol Psychiatry. 2010 Jan 15;67(2):146-54. doi: 10.1016/j.biopsych.2009.09.017.
7
Antidepressants increase neural progenitor cells in the human hippocampus.
Neuropsychopharmacology. 2009 Oct;34(11):2376-89. doi: 10.1038/npp.2009.75. Epub 2009 Jul 15.
9
Ageing abolishes the effects of fluoxetine on neurogenesis.
Mol Psychiatry. 2009 Sep;14(9):856-64. doi: 10.1038/mp.2008.147. Epub 2009 Jan 13.

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