THE EFFECT OF CHRONIC TREATMENT WITH IMIPRAMINE ON THE RESPONSIVENESS OF HIPPOCAMPAL CA1 NEURONS TO PHENYLEPHRINE AND SEROTONIN IN A CHRONIC MILD STRESS MODEL OF DEPRESSION
THE EFFECT OF CHRONIC TREATMENT WITH IMIPRAMINE ON THE RESPONSIVENESS OF HIPPOCAMPAL CA1 NEURONS TO PHENYLEPHRINE AND SEROTONIN IN A CHRONIC MILD STRESS MODEL OF DEPRESSION
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DOI：
10.1016/0924-977x(94)00132-u
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发表时间：
1995-03-01
影响因子：
5.6
通讯作者：
PAPP, M
中科院分区：
文献类型：
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作者：
BIJAK, M;PAPP, M
在大鼠海马切片的 CA1 细胞层中，体外检查了慢性轻度应激 (CMS) 和三环类抗抑郁药物丙咪嗪 (10 mg/kg/天，持续 5 周) 的长期治疗对神经元对 α1-去甲肾上腺素能激动剂去氧肾上腺素和血清素 (5-HT) 反应的影响。我们证实了之前的一些发现，即 CMS（曾被用作抑郁症动物模型）减少了 1% 蔗糖溶液的消耗，并且长期服用丙咪嗪可以逆转这种效果。丙咪嗪没有改变对照动物的蔗糖消耗量。在对照动物和应激动物中，去氧肾上腺素（5μM）和5-HT（10μM）减弱了通过刺激Schaffer侧支/连合纤维在CA1锥体细胞层中引起的群体峰值的幅度。长期使用丙咪嗪治疗可显着增强去氧肾上腺素和 5-HT 的抑制作用。对照动物和应激动物的切片中丙咪嗪诱导的增强作用相似。这些结果表明，丙咪嗪引起的海马α1-去甲肾上腺素能和5-羟色胺受体的功能变化并不参与抑郁症CMS模型中长期服用丙咪嗪的抗快感缺乏作用。
The effect of chronic mild stress (CMS) and chronic treatment with the tricyclic antidepressant drug imipramine (10 mg/kg/day for 5 weeks) on neuronal responsiveness to the alpha 1-noradrenergic agonist phenylephrine and serotonin (5-HT) was examined ex vivo, in the CA1 cell layer of the rat hippocampal slice preparation. We corroborated some previous findings that CMS, which had been used as an animal model of depression, decreased the consumption of a 1% sucrose solution and that that effect was reversed by chronic administration of imipramine. Imipramine did not change the sucrose consumption in control animals. In both control and stressed animals, phenylephrine (5 mu M) and 5-HT (10 mu M) attenuated the amplitude of the population spikes evoked in the CA1 pyramidal cell layer by stimulation of Schaffer collateral/commissural fibers. Those inhibitory effects of phenylephrine and 5-HT were significantly potentiated by chronic treatment with imipramine. The Imipramine-induced potentiation was similar in slices from control and stressed animals. These results suggest that the imipramine-induced functional changes in alpha 1-noradrenergic and serotonergic receptors in the hippocampus are not involved in the anti-anhedonic effect of chronic imipramine administration in the CMS model of depression.