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慢性尼古丁治疗可降低大鼠基底神经节中多巴胺D2激动剂的结合。

Chronic nicotine treatment decreases dopamine D2 agonist binding in the rat basal ganglia.

作者信息

Janson A M, Hedlund P B, Hillefors M, von Euler G

机构信息

Department of Histology and Neurobiology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Neuroreport. 1992 Dec;3(12):1117-20. doi: 10.1097/00001756-199212000-00021.

Abstract

To elucidate possible actions of nicotine on dopamine D2 receptor binding, the effect of chronic continuous (-)nicotine treatment (osmotic pumps s.c., 0.125 mg kg h-2, 14 days) was studied in the binding of [3H]N-propylnorapomorphine ([3H]NPA) and [125I]sulpride in coronal cryostat sections in the rat. Quantitative autoradiography showed that nicotine decreased the binding of [3H]NPA in the basal ganglia, preferentially in the nucleus accumbens and olfactory tubercle. In contrast, [125I]sulpride binding was not affected. Nicotine decreased the KD value of [3H]NPA by 27% and decreased the Bmax value by 17%, using filter-wiped sections. These results indicate that chronic continuous nicotine treatment affects the D2 receptor and that this effect may be involved in the development of nicotine dependence.

摘要

为阐明尼古丁对多巴胺D2受体结合的可能作用,研究了慢性持续(-)尼古丁治疗(皮下植入渗透泵,0.125毫克/千克/小时,14天)对大鼠冠状低温切片中[3H]N-丙基去甲阿朴吗啡([3H]NPA)和[125I]舒必利结合的影响。定量放射自显影显示,尼古丁降低了基底神经节中[3H]NPA的结合,优先降低了伏隔核和嗅结节中的结合。相比之下,[125I]舒必利的结合未受影响。使用滤膜擦拭切片,尼古丁使[3H]NPA的KD值降低了27%,使Bmax值降低了17%。这些结果表明,慢性持续尼古丁治疗会影响D2受体,且这种作用可能与尼古丁依赖的形成有关。

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