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发育过程中脑多巴胺缺乏会通过影响D1-多巴胺受体功能增加攻击和自伤行为易感性的证据。

Evidence that lack of brain dopamine during development can increase the susceptibility for aggression and self-injurious behavior by influencing D1-dopamine receptor function.

作者信息

Breese G R, Criswell H E, Mueller R A

机构信息

Brain and Development Research Center, University of North Carolina, School of Medicine, Chapel Hill.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 1990;14 Suppl:S65-80. doi: 10.1016/0278-5846(90)90089-y.

DOI:10.1016/0278-5846(90)90089-y
PMID:1982973
Abstract
  1. Lesch-Nyhan disease has a defined neurological lesion that is accompanied by abnormal motor function, aggression and self-injurious behavior. 2. The dopamine deficiency in Lesch-Nyhan disease has been modelled by destroying dopamine-containing neurons in neonatal rats with 6-hydroxydopamine. 3. Because D1-dopamine antagonists will block self-injurious behavior induced by L-DOPA in neonatal-6-OHDA-lesioned rats, D1-dopamine antagonists are proposed as a potential therapy for aggression and self-injurious behavior in patients with these symptoms. 4. The determination that the drug SCH-12679, which exhibited effectiveness against aggressiveness in mentally retarded patients, is a D1-dopamine antagonist supports the view that new D1-dopamine antagonists being developed will be an effective therapy for some types of aberrant behavior in this population.
摘要
  1. 莱施-奈恩病有明确的神经病变,伴有异常的运动功能、攻击行为和自我伤害行为。2. 通过用6-羟基多巴胺破坏新生大鼠中含多巴胺的神经元,对莱施-奈恩病中的多巴胺缺乏进行了模拟。3. 由于D1-多巴胺拮抗剂会阻断新生6-OHDA损伤大鼠中左旋多巴诱导的自我伤害行为,因此有人提出D1-多巴胺拮抗剂可作为治疗有这些症状患者的攻击行为和自我伤害行为的潜在疗法。4. 药物SCH-12679对智障患者的攻击性表现出有效性,该药物是一种D1-多巴胺拮抗剂,这支持了以下观点:正在研发的新型D1-多巴胺拮抗剂将成为治疗该人群某些类型异常行为的有效疗法。

相似文献

1
Evidence that lack of brain dopamine during development can increase the susceptibility for aggression and self-injurious behavior by influencing D1-dopamine receptor function.发育过程中脑多巴胺缺乏会通过影响D1-多巴胺受体功能增加攻击和自伤行为易感性的证据。
Prog Neuropsychopharmacol Biol Psychiatry. 1990;14 Suppl:S65-80. doi: 10.1016/0278-5846(90)90089-y.
2
Neurobiology of D1 dopamine receptors after neonatal-6-OHDA treatment: relevance to Lesch-Nyhan disease.新生期6-羟基多巴胺治疗后D1多巴胺受体的神经生物学:与莱施-奈恩病的相关性
Adv Exp Med Biol. 1986;204:197-215. doi: 10.1007/978-1-4684-5191-7_13.
3
Pharmacological evaluation of SCH-12679: evidence for an in vivo antagonism of D1-dopamine receptors.SCH-12679的药理学评估:D1-多巴胺受体体内拮抗作用的证据。
J Pharmacol Exp Ther. 1990 Feb;252(2):558-67.
4
D1 dopamine receptor-mediated substance P depletion in the striatonigral neurons of rats subjected to neonatal dopaminergic denervation: implications for self-injurious behavior.新生期多巴胺能去神经支配大鼠纹状体黑质神经元中D1多巴胺受体介导的P物质耗竭:对自伤行为的影响
Brain Res. 1989 Oct 23;500(1-2):119-30. doi: 10.1016/0006-8993(89)90305-3.
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A dopamine deficiency model of Lesch-Nyhan disease--the neonatal-6-OHDA-lesioned rat.莱施-奈恩病的多巴胺缺乏模型——新生6-羟基多巴胺损伤大鼠。
Brain Res Bull. 1990 Sep;25(3):477-84. doi: 10.1016/0361-9230(90)90240-z.
6
Comparison of the D1-dopamine agonists SKF-38393 and A-68930 in neonatal 6-hydroxydopamine-lesioned rats: behavioral effects and induction of c-fos-like immunoreactivity.D1-多巴胺激动剂SKF-38393和A-68930对新生6-羟基多巴胺损伤大鼠的比较:行为影响及c-fos样免疫反应性的诱导
J Pharmacol Exp Ther. 1992 Aug;262(2):855-65.
7
Monkeys with unilateral ventromedial tegmental lesions of the brain stem: models for Parkinson's disease and Lesch-Nyhan syndrome.患有单侧脑干腹内侧被盖区损伤的猴子:帕金森病和莱施-尼汉综合征的模型。
Prog Neuropsychopharmacol Biol Psychiatry. 1989;13(3-4):311-8. doi: 10.1016/0278-5846(89)90120-6.
8
6-hydroxydopamine treatments enhance behavioral responses to intracerebral microinjection of D1- and D2-dopamine agonists into nucleus accumbens and striatum without changing dopamine antagonist binding.6-羟基多巴胺处理增强了对向伏隔核和纹状体内脑微量注射D1和D2多巴胺激动剂的行为反应,而不改变多巴胺拮抗剂结合。
J Pharmacol Exp Ther. 1987 Jan;240(1):167-76.
9
Self-injurious behavior and dopaminergic neuron system in neonatal 6-hydroxydopamine-lesioned rat: 2. Intracerebral microinjection of dopamine agonists and antagonists.新生6-羟基多巴胺损伤大鼠的自伤行为与多巴胺能神经元系统:2. 脑室内微量注射多巴胺激动剂和拮抗剂
J Pharmacol Exp Ther. 1997 Feb;280(2):1031-7.
10
Effects of D1 and D2 dopamine receptor stimulation on the activity of substantia nigra pars reticulata neurons in 6-hydroxydopamine lesioned rats: D1/D2 coactivation induces potentiated responses.D1和D2多巴胺受体刺激对6-羟基多巴胺损伤大鼠黑质网状部神经元活动的影响:D1/D2共同激活诱导增强反应。
Brain Res. 1987 Mar 10;405(2):234-46. doi: 10.1016/0006-8993(87)90293-9.

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