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可卡因对伏隔核核心区和壳区的谷氨酸脱羧酶有不同影响。

Cocaine alters glutamic acid decarboxylase differentially in the nucleus accumbens core and shell.

作者信息

Sorg B A, Guminski B J, Hooks M S, Kalivas P W

机构信息

Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164-6520, USA.

出版信息

Brain Res Mol Brain Res. 1995 Apr;29(2):381-6. doi: 10.1016/0169-328x(94)00281-i.

Abstract

The effects of acute and repeated daily cocaine on the levels of mRNA coding for glutamic acid decarboxylase (GAD), preproenkephalin (PPE), preprotachykinin (PPT), and the dopamine D2 receptor were determined in the striatum, nucleus accumbens core and shell areas (NAcore, NAshell), and medial prefrontal cortex. Rats were given repeated saline or cocaine for 6 days. A cocaine challenge administered 24 h later resulted in an augmented locomotor response in daily cocaine-pretreated rats. Six h after the challenge, rats were sacrificed and Northern blot analysis revealed that acute cocaine increased GAD mRNA levels by 44% in the NAshell, while repeated cocaine prevented the acute cocaine-induced increase. These data suggest that cocaine may differentially regulate GABA release at NA core and shell projection fields.

摘要

研究了急性和每日重复给予可卡因对纹状体、伏隔核核心区和壳区(NAcore、NAshell)以及内侧前额叶皮质中编码谷氨酸脱羧酶(GAD)、前脑啡肽原(PPE)、前速激肽原(PPT)和多巴胺D2受体的mRNA水平的影响。给大鼠连续6天重复注射生理盐水或可卡因。24小时后给予可卡因激发,结果显示每日接受可卡因预处理的大鼠出现运动反应增强。激发后6小时,处死大鼠,Northern印迹分析显示,急性给予可卡因使NAshell中GAD mRNA水平增加44%,而重复给予可卡因则可阻止急性可卡因诱导的增加。这些数据表明,可卡因可能对NA核心区和壳区投射场的GABA释放有不同的调节作用。

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