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首页> 美国卫生研究院文献>other >Estradiol induces physical association of neuronal nitric oxide synthase with NMDA receptor and promotes nitric oxide formation via estrogen receptor activation in primary neuronal cultures
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Estradiol induces physical association of neuronal nitric oxide synthase with NMDA receptor and promotes nitric oxide formation via estrogen receptor activation in primary neuronal cultures

机译：雌二醇诱导神经元一氧化氮合酶与NMDA受体的物理缔合并通过初级神经元培养物中的雌激素受体激活促进一氧化氮形成。

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摘要

Estrogens and nitric oxide (NO) exert wide-ranging effects on brain function. Recent evidence suggested that one important mechanism for the regulation of NO production may reside in the differential coupling of the calcium-activated neuronal NO synthase (nNOS) to glutamate N-Methyl-D-Aspartate (NMDA) receptor channels harboring NR2B subunits by the scaffolding protein postsynaptic density-95 (PSD95), and that estrogens promote the formation of this ternary complex. Here, we demonstrate that 30-min estradiol-treatment triggers the production of NO by physically and functionally coupling NMDA receptors to nNOS in primary neurons of the rat preoptic region in vitro. The ability of estradiol to activate neuronal NO signaling in preoptic neurons and to promote changes in protein-protein interactions is blocked by ICI 182,780, an estrogen receptor antagonist. In addition, blockade of NMDA receptor NR2B subunit activity with ifenprodil or disruption of PSD95 synthesis in preoptic neurons by treatment with an antisense oligodeoxynucleotide inhibited the estradiol-promoted stimulation of NO release in cultured preoptic neurons. Thus, estrogen receptor-mediated stimulation of the nNOS/PSD95/NMDA receptor complex assembly is likely to be a critical component of the signaling process by which estradiol facilitates coupling of glutamatergic fluxes for NO production in neurons.
机译：雌激素和一氧化氮（NO）对脑功能产生广泛影响。最近的证据表明，调节NO产生的一种重要机制可能在于钙激活神经元NO合酶（nNOS）与谷氨酸N-甲基-D-天冬氨酸（NMDA）受体通道通过支架的差异偶联。蛋白突触后密度95（PSD95），而雌激素促进这种三元复合物的形成。在这里，我们证明了30分钟的雌二醇处理可通过将NMDA受体物理和功能耦合到大鼠视前区初级神经元中的nNOS触发NO的产生。雌激素激活视前神经元中神经元NO信号并促进蛋白-蛋白相互作用改变的能力被雌激素受体拮抗剂ICI 182,780阻断。此外，通过用反义寡聚脱氧核苷酸处理来抑制艾芬地尔对NMDA受体NR2B亚单位活性的阻滞或破坏视前神经元中的PSD95合成，可抑制雌二醇促进的培养视前神经元中NO的刺激。因此，雌激素受体介导的nNOS / PSD95 / NMDA受体复合物组装的刺激很可能是信号传导过程的关键组成部分，雌二醇通过该过程促进了谷氨酸能通量的耦合以产生神经元。

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