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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Genetic and pharmacological disruption of neurokinin, 1 receptor function decreases anxiety-related behaviors and increases serotonergic function
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Genetic and pharmacological disruption of neurokinin, 1 receptor function decreases anxiety-related behaviors and increases serotonergic function

机译：神经激肽的遗传和药理学破坏，1受体功能降低了焦虑相关行为并增加了血清素能功能

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摘要

Alterations in serotonin (5-hydroxytriptamine, 5-HT), norepineph- rine, and γ-aminobutyric acid have been linked to the pathophys- iology of anxiety and depression. and medications that modulate these neurotransmitters are widely used to treat mood disorders. Recently, the neuropeptide substance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), have been proposed as possible targets for new antidepressant and anxiolytic therapies. However. animal and human studies have so far failed to provide a dear consensus on the role of SP in the modulation of emotional states. Here we show that both genetic disruption and acute pharmaco- logical blockade of the NK1R in mice result in a marked reduction of anxiety and stress-related responses. These behavioral changes are paralleled by an increase in the firing rate of 5-HT neurons in the dorsal raphe nucleus, a major source of serotonergic input to the forebrain. NK1R disruption also results in a selective desensi- tization of 5-HT1A inhibitory autoreceptors, which resembles the effect of sustained antidepressant treatment. Together these re- sults indicate that the SP system powerfully modulates anxiety and suggest that this effect is at least in part mediated by changes in the 5-HT system.
机译：血清素（5-羟基三甲胺，5-HT），去甲肾上腺素和γ-氨基丁酸的改变与焦虑和抑郁症的病理学有关。调节这些神经递质的药物被广泛用于治疗情绪障碍。最近，已经提出了神经肽物质P（SP）及其受体神经激肽1受体（NK1R）作为新的抗抑郁和抗焦虑疗法的可能靶标。然而。迄今为止，动物和人体研究未能就SP在调节情绪状态中的作用达成共识。在这里，我们表明，NK1R的遗传破坏和急性药物阻断均能显着降低焦虑和压力相关反应。这些行为改变与背缝核中5-HT神经元的放电速率增加平行，背缝核是前脑血清素输入的主要来源。 NK1R的破坏还导致5-HT1A抑制性自体受体的选择性脱敏，类似于持续抗抑郁药治疗的效果。这些结果共同表明SP系统可以有效地调节焦虑，并表明这种作用至少部分是由5-HT系统的变化介导的。

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