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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 >Cortical alpha-adrenoceptor downregulation by tricyclic antidepressants in the rat brain.
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Cortical alpha-adrenoceptor downregulation by tricyclic antidepressants in the rat brain.

机译：三环抗抑郁药在大鼠大脑中的皮质α肾上腺素受体下调。

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The aim of the present study was to examine the effect of chronic tricyclic antidepressants (TCAs) treatment on the density of alpha-adrenoceptors in the rat brain. Density of alpha1- and alpha2-adrenoceptors was measured in cortex and hippocampus of rats treated with imipramine (IMI, 5mg/kg body weight), desipramine (DMI, 10mg/kg body weight), clomipramine (CMI, 10mg/kg body weight) and amitriptyline (AMI, 10mg/kg body weight), for 40 days, using [3H]prazosin and [3H]clonidine, respectively. The density of cortical alpha1-adrenoceptors was significantly decreased with IMI (46%), DMI (21%), CMI (50%) and AMI (67%) treatment, without altering the affinity of the receptor. The density of cortical alpha2-adrenoceptors was also significantly decreased with DMI (69%), CMI (81%) and AMI (80%) treatment, without affecting the affinity for [3H]clonidine. The density of hippocampal alpha1-adrenoceptors was significantly decreased only with AMI treatment (47%), without affecting the affinity for [3H]prazosin. However, no change in hippocampal alpha2-adrenoceptor density was observed with any of these TCAs. The results suggest that chronic antidepressant (AD) treatment downregulates the cortical, but not hippocampal, alpha1- and alpha2-adrenoceptors in rat brain. The region-specific downregulation of alpha1- and alpha2-adrenoceptors density, which occur after prolonged AD treatment, may underline the therapeutic mechanism of action.
机译：本研究的目的是研究慢性三环抗抑郁药（TCA）处理对大鼠大脑中α-肾上腺素受体密度的影响。在用丙咪嗪（IMI，5mg / kg体重），地昔帕明（DMI，10mg / kg体重），氯米帕明（CMI，10mg / kg体重）治疗的大鼠的皮质和海马中测量α1-和α2-肾上腺素受体的密度。和[阿米替林]（AMI，10mg / kg体重），分别使用[3H]哌唑嗪和[3H]可乐定治疗40天。 IMI（46％），DMI（21％），CMI（50％）和AMI（67％）处理可显着降低皮质α1-肾上腺素受体的密度，而不会改变受体的亲和力。 DMI（69％），CMI（81％）和AMI（80％）处理也显着降低了皮质α2-肾上腺素受体的密度，而没有影响对[3H]可乐定的亲和力。仅通过AMI治疗，海马α1-肾上腺素受体的密度显着降低（47％），而不会影响对[3H]普拉唑星的亲和力。但是，这些TCA均未观察到海马α2-肾上腺素受体密度的变化。结果表明，慢性抗抑郁药（AD）下调大鼠大脑皮质，但不是海马中的α1和α2肾上腺素受体。长时间AD治疗后发生的α1-和α2-肾上腺素受体密度的区域特异性下调可能强调了治疗的作用机理。

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