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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Differential effects of the antidepressant mirtazapine on amphetamine- and dizocilpine-induced PPI deficits
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Differential effects of the antidepressant mirtazapine on amphetamine- and dizocilpine-induced PPI deficits

机译：抗抑郁药米氮平对苯丙胺和地佐西平诱导的PPI缺陷的差异作用

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Prepulse inhibition (PPI) refers to the decrease in motor startle response to salient sensory stimuli (pulses) when they are closely preceded in time by another more modest sensory stimulus (prepulse). PPI deficits can be induced by stimulation of dopamine receptors (e.g., amphetamine or apomorphine) or blockade of NMDA glutamate receptors (e.g., dizocilpine or PCP). Previously we found that antagonists of α 2-noradrenergic and H 1-histaminergic receptors significantly attenuate PPI impairments caused by amphetamine or dizocilpine. In the current study we assessed the effects of the antidepressant mirtazapine, which has combined antagonist effects at α 2-noradrenergic, H 1-histaminergic and 5-HT serotonergic receptors, on amphetamine- and dizocilpine-induced PPI deficits. In Experiment 1, rats were tested for PPI of the startle response to a tactile air-puff stimulus after auditory prepulses of three different intensities. Drug treatments consisted of combinations of amphetamine (0 and 1mg/kg) and mirtazapine (0, 0.5, 1, 2, and 5mg/kg), with all rats receiving all drug doses and combinations with different counterbalanced orders. In Experiment 2, a different group of rats was tested with drug treatments consisting of combinations of dizocilpine (0 and 0.05mg/kg) and mirtazapine (0, 0.5, 1, 2, and 5mg/kg). In Experiment 1 amphetamine (1mg/kg) significantly reduced PPI whereas mirtazapine caused the opposite effect, with the highest dose of mirtazapine (5mg/kg) effectively reversing the amphetamine-induced PPI deficit. In Experiment 2 dizocilpine (0.05mg/kg) significantly reduced PPI, but mirtazapine did not have a significant effect on the inhibition of the startle response. These results indicate that the potential beneficial effects of combined α-adrenergic, 5-HT, and H 1 receptor blockade in counteracting PPI deficits may be associated to cases of sensorimotor gating disorders mediated by dopamine, but not necessarily to NMDA glutamate-induced PPI impairments.
机译：前脉冲抑制（PPI）是指在紧挨着另一个更适度的感觉刺激（预脉冲）的时间之前，对突显感觉刺激（脉冲）的运动惊吓反应的减少。可通过刺激多巴胺受体（例如苯丙胺或阿扑吗啡）或阻断NMDA谷氨酸受体（例如地佐西平或PCP）来诱发PPI缺乏。先前我们发现，α2-去甲肾上腺素能受体和H 1-组胺能受体的拮抗剂可显着减轻由苯丙胺或地佐西平引起的PPI损伤。在本研究中，我们评估了抗抑郁药米氮平对苯丙胺和地佐西平诱导的PPI缺乏的综合作用，该组合对α2-去甲肾上腺素能，H 1-组胺能和5-HT血清素能受体具有拮抗作用。在实验1中，测试了老鼠在三种不同强度的听觉预脉冲后对触觉气喘刺激产生的惊吓反应的PPI。药物治疗包括苯丙胺（0和1mg / kg）和米氮平（0、0.5、1、2和5mg / kg）的组合，所有大鼠均接受所有药物剂量和具有不同平衡顺序的组合。在实验2中，对另一组大鼠进行了药物治疗，其中包括地佐西平（0和0.05mg / kg）和米氮平（0、0.5、1、2和5mg / kg）的组合。在实验1中，苯丙胺（1mg / kg）显着降低了PPI，而米氮平则产生了相反的作用，最高剂量的米氮平（5mg / kg）有效地逆转了苯丙胺引起的PPI不足。在实验2中，地佐西平（0.05mg / kg）显着降低了PPI，但米氮平对惊吓反应的抑制作用不明显。这些结果表明，联合使用α-肾上腺素，5-HT和H 1受体阻滞剂可抵消PPI缺陷，可能与多巴胺介导的感觉运动门控障碍有关，但不一定与NMDA谷氨酸诱导的PPI损伤有关。

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