Basheer R, Halldner L, Alanko L, McCarley R W, Fredholm B B, Porkka-Heiskanen T
Harvard Medical School and V.A. Medical Center, Department of Psychiatry, West Roxbury, MA 02132, USA.
Neuroreport. 2001 Jun 13;12(8):1577-80. doi: 10.1097/00001756-200106130-00013.
Extracellular levels of adenosine increase in basal forebrain following prolonged wakefulness. Moreover, perfusion of adenosine into basal forebrain increases sleep. In this study we have examined the adenosine receptor subtypes, A1 and A2A, for changes in the levels of mRNA using RT-PCR and in situ hybridization and the receptor ligand binding efficiency using autoradiography following 3 and 6 h of sleep deprivation. We observed that A1 receptor mRNA levels increased in basal forebrain with no changes in other forebrain areas examined. A1 receptor binding was not affected. A2A receptor mRNA and ligand binding were undetectable in basal forebrain. However, in the olfactory tubercle, A2A mRNA and receptor binding decreased significantly. Based on the significant increase in the A1 but not in A2A receptor, we hypothesize that the effects of sleep deprivation-induced increased adenosine are mediated by A1 receptor in basal forebrain of rats.
长时间清醒后,基底前脑的细胞外腺苷水平会升高。此外,向基底前脑灌注腺苷会增加睡眠。在本研究中,我们使用逆转录聚合酶链反应(RT-PCR)和原位杂交技术检测了腺苷受体亚型A1和A2A的mRNA水平变化,并在睡眠剥夺3小时和6小时后使用放射自显影技术检测了受体配体结合效率。我们观察到,基底前脑的A1受体mRNA水平升高,而在所检测的其他前脑区域没有变化。A1受体结合不受影响。在基底前脑中未检测到A2A受体mRNA和配体结合。然而,在嗅结节中,A2A mRNA和受体结合显著降低。基于A1受体而非A2A受体的显著增加,我们推测睡眠剥夺诱导的腺苷增加的作用是由大鼠基底前脑中的A1受体介导的。