去甲肾上腺素能损伤可拮抗地昔帕明诱导的NMDA受体适应性变化。
Noradrenergic lesion antagonizes desipramine-induced adaptation of NMDA receptors.
作者信息
Harkin A, Nowak G, Paul I A
机构信息
Laboratory of Neurobehavioral Pharmacology, Division of Neurobiology and Behavior Research, Department of Psychiatry, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
出版信息
Eur J Pharmacol. 2000 Feb 18;389(2-3):187-92. doi: 10.1016/s0014-2999(99)00923-1.
Repeated administration of the tricyclic antidepressant, desipramine, for 28 days to mice effected a decrease in the potency of glycine to displace [3H]5,7-dichlorokynurenic acid (5,7-DCKA) in mouse cortical homogenates. Pre-treatment with the noradrenergic neurotoxin DSP-4, while having no effect alone, attenuated the desipramine-induced effect. The present findings support a norepinephrine-dependent adaptation of the NMDA receptor complex in vivo following chronic desipramine treatment. The inter-relationship of norepinephrine and glutamate transmission may provide insight into the mechanism underlying the action of antidepressant drugs.
给小鼠反复服用三环类抗抑郁药地昔帕明28天，导致小鼠皮质匀浆中甘氨酸置换[3H]5,7-二氯犬尿喹啉酸（5,7-DCKA）的能力下降。用去甲肾上腺素能神经毒素DSP-4预处理，虽然单独使用时没有效果，但减弱了地昔帕明诱导的效应。目前的研究结果支持慢性地昔帕明治疗后体内NMDA受体复合物的去甲肾上腺素依赖性适应性变化。去甲肾上腺素与谷氨酸传递之间的相互关系可能有助于深入了解抗抑郁药物作用的潜在机制。
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