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本文引用的文献

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Sprague-Dawley and Fischer female rats differ in acute effects of fluoxetine on sexual behavior.Sprague-Dawley 和 Fischer 雌性大鼠在氟西汀对性行为的急性影响方面存在差异。
J Sex Med. 2013 Feb;10(2):350-61. doi: 10.1111/j.1743-6109.2012.02981.x. Epub 2012 Oct 30.
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Understanding the molecular pharmacology of the serotonergic system: using fluoxetine as a model.理解血清素能系统的分子药理学:以氟西汀为模型。
J Pharm Pharmacol. 2012 Mar;64(3):317-25. doi: 10.1111/j.2042-7158.2011.01384.x. Epub 2011 Nov 18.
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Role of 5-HT(1A) receptors in fluoxetine-induced lordosis inhibition.5-HT(1A) 受体在氟西汀诱导的摆臀抑制中的作用。
Horm Behav. 2010 Jul;58(2):290-6. doi: 10.1016/j.yhbeh.2010.03.003. Epub 2010 Mar 8.
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Fluoxetine (Prozac) binding to serotonin transporter is modulated by chloride and conformational changes.氟西汀(百忧解)与血清素转运蛋白的结合受氯离子和构象变化的调节。
J Neurosci. 2009 Jul 29;29(30):9635-43. doi: 10.1523/JNEUROSCI.0440-09.2009.
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Modest effects of repeated fluoxetine on estrous cyclicity and sexual behavior in Sprague Dawley female rats.重复给予氟西汀对斯普拉格-道利雌性大鼠发情周期和性行为的适度影响。
Brain Res. 2008 Dec 15;1245:52-60. doi: 10.1016/j.brainres.2008.09.063. Epub 2008 Oct 2.
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Investigation of the SSRI augmentation properties of 5-HT(2) receptor antagonists using in vivo microdialysis.使用体内微透析法研究5-羟色胺(2)受体拮抗剂的选择性5-羟色胺再摄取抑制剂增强特性。
Neuropharmacology. 2006 May;50(6):726-32. doi: 10.1016/j.neuropharm.2005.11.020. Epub 2006 Jan 23.
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Burden of phase-specific sexual dysfunction with SSRIs.选择性5-羟色胺再摄取抑制剂(SSRI)所致阶段性性功能障碍的负担
J Affect Disord. 2006 Mar;91(1):27-32. doi: 10.1016/j.jad.2005.12.007. Epub 2006 Jan 20.
8
Fluoxetine disrupts food intake and estrous cyclicity in Fischer female rats.氟西汀会扰乱费希尔雌性大鼠的食物摄入和发情周期。
Brain Res. 2006 Feb 9;1072(1):79-90. doi: 10.1016/j.brainres.2005.12.033. Epub 2006 Jan 19.
9
A role for midbrain raphe gamma aminobutyric acid neurons in 5-hydroxytryptamine feedback control.中脑缝际γ-氨基丁酸能神经元在5-羟色胺反馈控制中的作用。
Neuroreport. 2005 Jun 21;16(9):891-6. doi: 10.1097/00001756-200506210-00004.
10
The selective 5-HT2A receptor antagonist M100907 enhances antidepressant-like behavioral effects of the SSRI fluoxetine.选择性5-羟色胺2A受体拮抗剂M100907增强了选择性5-羟色胺再摄取抑制剂氟西汀的抗抑郁样行为效应。
Neuropsychopharmacology. 2005 Dec;30(12):2205-15. doi: 10.1038/sj.npp.1300762.

比较雌性 Fischer 和 Sprague-Dawley 大鼠对酮色林的反应。

Comparison of female Fischer and Sprague-Dawley rats in the response to ketanserin.

机构信息

Department of Biology, Texas Woman's University, Denton, TX 76204, United States.

出版信息

Pharmacol Biochem Behav. 2013 Dec;114-115:52-7. doi: 10.1016/j.pbb.2013.10.024. Epub 2013 Nov 4.

DOI:10.1016/j.pbb.2013.10.024
PMID:24201045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3902122/
Abstract

The effects of the 5-HT2A/2C receptor antagonist, ketanserin, on lordosis behavior were examined in hormonally primed, ovariectomized Fischer and Sprague-Dawley females. Rats were primed with 0.067μg/g body weight estradiol benzoate and 3.33μg/g body weight progesterone. After a pretest for sexual behavior, rats were injected with 0.416 to 10mg/kg ketanserin. In both strains, lordosis behavior, lordosis quality, and proceptivity were significantly reduced by ketanserin. There was modest evidence of a strain difference with Sprague-Dawley females slightly more sensitive to ketanserin. In a second experiment, the effects of 10mg/kg fluoxetine, 1mg/kg ketanserin, and their combination were examined to determine if the two drugs would have additive effects on sexual behavior. There was no evidence that the drugs were additive in their effect and the strains did not differ in their response to the combined treatment. These findings are discussed in relation to prior evidence for strain differences in the sexual behavioral response to fluoxetine and to a receptor agonist acting preferentially at 5-HT1A receptors.

摘要

在激素诱导的去卵巢费希尔和斯普拉格-道利雌性大鼠中,研究了 5-HT2A/2C 受体拮抗剂酮色林对发情行为的影响。大鼠用 0.067μg/g 体重苯甲酸雌二醇和 3.33μg/g 体重孕酮诱导。在性行为预测试验后,大鼠注射 0.416 至 10mg/kg 酮色林。在两种品系中,酮色林显著降低了发情行为、发情质量和求爱性。有适度的证据表明存在品系差异,斯普拉格-道利雌性对酮色林的敏感性略高。在第二项实验中,检查了 10mg/kg 氟西汀、1mg/kg 酮色林及其组合对性行为的影响,以确定这两种药物在其对性行为的影响上是否具有相加作用。没有证据表明这些药物的作用具有相加性,而且两种品系对联合治疗的反应没有差异。这些发现与先前关于氟西汀对性行为反应的品系差异的证据以及对优先作用于 5-HT1A 受体的受体激动剂的证据有关。