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首页> 外文期刊>The European Journal of Neuroscience >5-HT(2C) antagonism blocks blood oxygen level-dependent pharmacological-challenge magnetic resonance imaging signal in rat brain areas related to feeding.
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5-HT(2C) antagonism blocks blood oxygen level-dependent pharmacological-challenge magnetic resonance imaging signal in rat brain areas related to feeding.

机译：5-HT（2C）拮抗作用可阻断与进食相关的大鼠脑区域中血氧水平依赖的药理挑战磁共振成像信号。

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In this study, pharmacological-challenge magnetic resonance imaging was used to further characterize the central action of serotonin on feeding. In both feeding and pharmacological-challenge magnetic resonance imaging experiments, we combined 5-HT(1B/2C) agonist m-chlorophenylpiperazine (mCPP) challenge with pre-treatment with the selective 5-HT(1B) and 5-HT(2C) receptor antagonists, SB 224289 (2.5 mg/kg) and SB 242084 (2 mg/kg), respectively. Subcutaneous injection of mCPP (3 mg/kg) completely blocked fast-induced refeeding in freely behaving, non-anaesthetized male rats, an effect that was not modified by the 5-HT(1B) receptor antagonist but was partially reversed by the 5-HT(2C) receptor antagonist. mCPP alone induced both positive and negative blood oxygen level-dependent (BOLD) responses in the brains of anaesthetized rats, including in the limbic system and basal ganglia. Overall, the 5-HT(2C) antagonist SB 242084 reversed the effects elicited by mCPP, whereas the 5-HT(1B) antagonist SB 224289 had virtually no impact. SB 242084 eliminated BOLD signal in nuclei associated with the limbic system and diminished activation in basal ganglia. In addition, BOLD signal was returned to baseline levels in the cortical regions and cerebellum. These results suggest that mCPP may reduce food intake by acting specifically on brain circuits that are modulated by 5-HT(2C) receptors in the rat.
机译：在这项研究中，使用药理学挑战磁共振成像来进一步表征5-羟色胺对进食的中枢作用。在进食和药理挑战磁共振成像实验中，我们将5-HT（1B / 2C）激动剂间氯苯哌嗪（mCPP）激发与选择性5-HT（1B）和5-HT（2C）预处理相结合受体拮抗剂分别为SB 224289（2.5 mg / kg）和SB 242084（2 mg / kg）。皮下注射mCPP（3 mg / kg）完全阻断了自由行为，未麻醉的雄性大鼠的快速诱导的进食，该作用并未被5-HT（1B）受体拮抗剂改变，但被5-HT逆转了HT（2C）受体拮抗剂。单独使用mCPP会在麻醉大鼠的大脑中（包括在边缘系统和基底神经节中）诱发正负血液氧水平依赖性（BOLD）反应。总体而言，5-HT（2C）拮抗剂SB 242084逆转了mCPP引起的作用，而5-HT（1B）拮抗剂SB 224289实际上没有影响。 SB 242084消除了与边缘系统相关的细胞核中的BOLD信号，并减少了基底神经节的激活。此外，BOLD信号在皮质区域和小脑恢复到基线水平。这些结果表明，mCPP可能通过专门作用于大鼠中5-HT（2C）受体调节的脑回路而减少食物摄入。

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