谷氨酸及其受体在抑郁症病机和治疗中的作用研究进展

被引：12

作者：

王晓龙

张惠云

机构：

[1] 山东中医药大学中医药经典理论教育部重点实验室

来源：

医学研究杂志 | 2013年 / 42卷 / 09期

关键词：

D O I：

暂无

中图分类号：

R749.4 [情感性精神病];

学科分类号：

100204 [神经病学];

摘要：

<正>抑郁症是当前一种常见精神疾病,以情绪异常低落、思维迟滞和意志减退为主要表现,伴有多种精神、躯体症状,其中高达15%的患者具有自杀倾向,严重影响患者生活质量。关于抑郁症的病机假说众多,目前尚无统一定论。临床上常用的抗抑郁药大多基于抑郁症发病机制"生物胺假说"所研制,在药理作用、临床研究和不良反应等方面有相似之处,存在起效慢、复发率高、缓解率低和长期用药等不足。近年来,大量的研究表明谷氨酸受体调节剂在抗抑郁方面发

引用

页码：13 / 16

页数：4

共 15 条

[1]

Metabotropic glutamate 2/3 receptor antagonists improve behavioral and prefrontal dopaminergic alterations in the chronic corticosterone-induced depression model in mice.[J].Yukio Ago;Koji Yano;Ryota Araki;Naoki Hiramatsu;Yuki Kita;Toshiyuki Kawasaki;Hirotaka Onoe;Shigeyuki Chaki;Atsuro Nakazato;Hitoshi Hashimoto;Akemichi Baba;Kazuhiro Takuma;Toshio Matsuda.Neuropharmacology.2013,

[2]

Selective activation of either mGlu2 or mGlu3 receptors can induce LTD in the amygdala.[J].Sarah J. Lucas;Zuner A. Bortolotto;Graham L. Collingridge;David Lodge.Neuropharmacology.2012,

[3]

Genetic ablation of the GluK4 kainate receptor subunit causes anxiolytic and antidepressant-like behavior in mice.[J].Justin S. Catches;Jian Xu;Anis Contractor.Behavioural Brain Research.2011, 2

[4]

The mGluR7 allosteric agonist AMN082 produces antidepressant-like effects by modulating glutamatergic signaling.[J].Stefania Risso Bradley;Jason M. Uslaner;Rose B. Flick;Ariel Lee;Kristina M. Groover;Peter H. Hutson.Pharmacology; Biochemistry and Behavior.2011, 1

[5]

Kainate receptor-mediated depression of glutamatergic transmission involving protein kinase A in the lateral amygdala [J].

Vicente Negrete-Diaz, Jose ;

Duque-Feria, Paloma ;

Andrade-Talavera, Yuniesky ;

Carrion, Miriam ;

Flores, Gonzalo ;

Rodriguez-Moreno, Antonio .

JOURNAL OF NEUROCHEMISTRY, 2012, 121 (01) :36-43

[6]

The antidepressant-like effects of glutamatergic drugs ketamine and AMPA receptor potentiator LY 451646 are preserved in bdnf +/? heterozygous null mice.[J]..Neuropharmacology.2011, 1

[7]

Chronic antidepressant treatments induce a time-dependent up-regulation of AMPA receptor subunit protein levels [J].