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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Flesinoxan challenge suggests that chronic treatment with paroxetine in rats does not desensitize receptors controlling 5-HT synthesis.
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Flesinoxan challenge suggests that chronic treatment with paroxetine in rats does not desensitize receptors controlling 5-HT synthesis.

机译：Flesinoxan挑战表明，在大鼠中长期用帕罗西汀治疗不会使控制5-HT合成的受体脱敏。

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It has been proposed that the desensitization of 5-HT(1A) (5-hydroxytryptamine; serotonin) receptors following chronic therapy with selective serotonin reuptake inhibitors (SSRIs) is necessary for their therapeutic efficacy. Stimulation of the 5-HT(1A) receptors decreases serotonin (5-HT) synthesis and release, but it is not clear if the receptors are fully desensitized following chronic SSRI treatment. The main objective of this study was evaluation of ability of 5-HT(1A) receptors to modulate 5-HT synthesis after 14-day paroxetine treatment. 5-HT(1A) receptor sensitivity following chronic administration of the SSRI paroxetine was assessed by the ability of an acute challenge with the 5-HT(1A) agonist, flesinoxan, to modulate 5-HT synthesis in the rat brain. The rates of 5-HT synthesis were measured using the alpha-[(14)C]methyl-l-tryptophan autoradiographic method. The rats were treated for 2 weeks with paroxetine (10mg/(kgday), s.c., delivered by osmotic minipump). After this treatment, the rats received an acute challenge with flesinoxan (5mg/kg, i.p.), while the control rats were injected with the vehicle. Forty minutes following the flesinoxan injection, the tracer, alpha-[(14)C]methyl-l-tryptophan, was injected over 2min. 5-HT synthesis rates were calculated from autoradiographically measured tissue tracer concentrations and plasma time-activity curves. The results demonstrated that the acute flesinoxan challenge produced a significant decrease in 5-HT synthesis rates throughout the rat brain. The greatest decrease was observed in the ventral hippocampus, somatosensory cortex and the ascending serotonergic cell bodies. In comparison with data reported on an acute challenge with flesinoxan in naive rats (rats without any other treatment), the results presented here suggest a greater effect of flesinoxan on synthesis reduction in rats chronically treated with paroxetine. The results also suggest that the 5-HT receptors were not fully desensitized by paroxetine treatment, and that the stimulation of5-HT(1A) receptors with an agonist is still capable of reducing 5-HT synthesis.
机译：有人提出，对5-HT（1A）（5-羟色胺; 5-羟色胺）受体进行选择性5-羟色胺再摄取抑制剂（SSRIs）慢性治疗后脱敏是其治疗功效所必需的。 5-HT（1A）受体的刺激会降低血清素（5-HT）的合成和释放，但尚不清楚在慢性SSRI治疗后受体是否完全脱敏。这项研究的主要目的是评估14天帕罗西汀治疗后5-HT（1A）受体调节5-HT合成的能力。通过5-HT（1A）激动剂flesinoxan急性攻击调节大鼠大脑中5-HT合成的能力，评估了SSRI帕罗西汀长期给药后的5-HT（1A）受体敏感性。使用α-[（14）C]甲基-1-色氨酸放射自显影法测量5-HT的合成速率。用帕罗西汀（皮下注射10mg /（kg·day），皮下注射，通过渗透微型泵递送）治疗大鼠2周。经过这种处理后，大鼠接受了氟苯氧氟沙星（5mg / kg，腹腔注射）的急性攻击，而对照大鼠则被注射了赋形剂。注射氟西诺沙following后40分钟，在2分钟内注射了示踪剂α-[（14）C]甲基-1-色氨酸。从放射自显影测量的组织示踪剂浓度和血浆时间-活性曲线计算5-HT合成速率。结果表明，急性的flesinoxan攻击使整个大鼠大脑的5-HT合成速率显着降低。在腹侧海马，体感皮层和上升的血清素能细胞体中观察到最大的减少。与报道的在未使用过的大鼠（未经任何其他治疗的大鼠）中使用flesinoxan进行急性攻击的数据相比，此处显示的结果表明，在长期用帕罗西汀治疗的大鼠中，flesinoxan对合成减少有更大的作用。结果还表明，帕罗西汀治疗不能使5-HT受体完全脱敏，并且激动剂对5-HT（1A）受体的刺激仍然能够减少5-HT的合成。

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