Soria C, Fernandez-Lopez A, Gomez T, Calvo P
Department of Biochemistry and Molecular Biology, University of León, Spain.
Brain Res Bull. 1991 Nov;27(5):611-5. doi: 10.1016/0361-9230(91)90035-i.
Chronic morphine treatment produced increases in [3H]-flunitrazepam binding in some hippocampal areas of the rat brain. The differences in binding were statistically significant in some cases. Both morphine-dependent and morphine-deprived (abstinence syndrome) animals showed an identical response in binding, which confirms a real, although small, increase in benzodiazepine binding sites in the hippocampus after morphine treatment, that is not affected by a naloxone-induced abstinence syndrome under the conditions studied. These findings support the hypothesis of a morphine-induced up-regulation of benzodiazepine binding sites in the hippocampus. A possible different response in benzodiazepine binding sites 1 and 2 could explain the different findings reported in the literature. Our data suggest that the detected increase in benzodiazepine binding would be mainly due to type 2 binding sites, since the hippocampus has a higher density of this type of benzodiazepine binding sites.
慢性吗啡处理使大鼠脑海马某些区域的[3H] -氟硝西泮结合增加。在某些情况下，结合差异具有统计学意义。吗啡依赖和吗啡戒断（戒断综合征）动物在结合方面表现出相同的反应，这证实了吗啡处理后海马中苯二氮䓬结合位点确实存在增加，尽管增加幅度较小，并且在所研究的条件下不受纳洛酮诱导的戒断综合征影响。这些发现支持了吗啡诱导海马中苯二氮䓬结合位点上调的假说。苯二氮䓬结合位点1和2可能存在的不同反应可以解释文献中报道的不同结果。我们的数据表明，检测到的苯二氮䓬结合增加主要归因于2型结合位点，因为海马中这种类型的苯二氮䓬结合位点密度更高。
