Castelli M P, Melis M, Mameli M, Fadda P, Diaz G, Gessa G L
B.B. Brodie' Department of Neuroscience, University of Cagliari, Italy.
Brain Res Mol Brain Res. 1997 Apr;45(1):149-53. doi: 10.1016/s0169-328x(96)00305-1.
Previous radioligand-binding studies have reported conflicting results concerning the effect of chronic morphine administration on the regulation of mu-opioid receptor (MOR) density. On the other hand, chronic administration of an opioid antagonist, such as naltrexone, has been shown to increase the density of the MOR. In order to determine if the changes in the MOR are associated with alterations in receptor mRNA levels, we investigated MOR gene expression following chronic treatment with morphine and/or naltrexone. MOR mRNA levels, determined by the ribonuclease protection assay (RPA), were unchanged with respect to control during chronic morphine treatment and morphine withdrawal in each of the analysed brain areas. Furthermore, chronic administration of naltrexone did not result in changes of MOR mRNA levels in rat striatum of naive and morphine-dependent rats, suggesting that the up-regulation of the MOR density, at least in this tissue, is not regulated at transcriptional level.
以往的放射性配体结合研究报告了慢性吗啡给药对μ-阿片受体（MOR）密度调节作用的相互矛盾的结果。另一方面，已表明慢性给予阿片类拮抗剂，如纳曲酮，可增加MOR的密度。为了确定MOR的变化是否与受体mRNA水平的改变相关，我们研究了吗啡和/或纳曲酮慢性治疗后的MOR基因表达。通过核糖核酸酶保护分析（RPA）测定的MOR mRNA水平，在每个分析的脑区中，慢性吗啡治疗和吗啡戒断期间相对于对照没有变化。此外，在未接触过吗啡和吗啡依赖的大鼠纹状体中，慢性给予纳曲酮并未导致MOR mRNA水平的变化，这表明MOR密度的上调，至少在该组织中，不是在转录水平上调节的。
