Belachew S, Rogister B, Rigo J M, Malgrange B, Mazy-Servais C, Xhauflaire G, Coucke P, Moonen G
Department of Human Physiology and Pathophysiology, University of Liège, Belgium.
Eur J Neurosci. 1998 Nov;10(11):3556-64. doi: 10.1046/j.1460-9568.1998.00369.x.
Using the whole-cell patch-clamp technique, we demonstrate glycine-induced currents in oligosphere-derived oligodendrocyte progenitors cultured from newborn rats. Similar inward currents are also triggered by beta-alanine and taurine, two established glycine receptor agonists. In our recording conditions, glycine-gated currents in oligodendrocyte progenitors reverse about 0 mV and are reversibly inhibited by the glycine competitive antagonist strychnine, the Cl- channel blocker picrotoxinin and the non-competitive antagonist cyanotriphenylborate. The oligodendrocyte progenitors glycine receptor (GlyR) differs from the corresponding neuronal receptor: [3H]strychnine binding data and the strychnine inhibition curve of glycine-induced currents in oligodendrocyte progenitor cultures suggest the existence of two strychnine binding sites on the oligodendroglial GlyR. Using total RNA isolated from oligodendrocyte progenitors cultures, reverse transcription-polymerase chain reaction analysis of glycine receptor subunit expression shows the presence of alpha2 and beta subunits and immunocytochemical stainings confirm that this GlyR contains an alpha subunit which is not alpha1. The molecular structure of the oligodendroglial GlyR could be either homopentameric alpha2 or heteromeric alpha2beta but in both cases, the sequence of the alpha2 or beta subunits have to be different from the known neuronal sequences in order to explain, respectively, the cyanotriphenylborate (alpha2) and picrotoxinin (beta) sensitivities. This work thus demonstrates that GlyR are expressed by oligodendrocytes obtained not only from spinal cord but also from supraspinal structures. The pharmacological properties and presumably the molecular structure of oligodendroglial GlyR are original. The physiological meaning of the presence of such receptors on developing and mature oligodendrocytes remains unknown.
运用全细胞膜片钳技术，我们在新生大鼠来源的少突胶质前体细胞培养的寡球中证实了甘氨酸诱导的电流。β-丙氨酸和牛磺酸这两种已确定的甘氨酸受体激动剂也能引发类似的内向电流。在我们的记录条件下，少突胶质前体细胞中的甘氨酸门控电流在约0 mV处反转，并被甘氨酸竞争性拮抗剂士的宁、氯离子通道阻滞剂印防己毒素和非竞争性拮抗剂氰化三苯硼酸盐可逆性抑制。少突胶质前体细胞甘氨酸受体（GlyR）与相应的神经元受体不同：[3H]士的宁结合数据以及少突胶质前体细胞培养物中甘氨酸诱导电流的士的宁抑制曲线表明，少突胶质细胞的GlyR上存在两个士的宁结合位点。利用从少突胶质前体细胞培养物中分离的总RNA，对甘氨酸受体亚基表达进行逆转录-聚合酶链反应分析，结果显示存在α2和β亚基，免疫细胞化学染色证实该GlyR包含一个非α1的α亚基。少突胶质细胞GlyR的分子结构可能是同五聚体α2或异聚体α2β，但在这两种情况下，α2或β亚基的序列都必须与已知的神经元序列不同，以便分别解释氰化三苯硼酸盐（α2）和印防己毒素（β）的敏感性。因此，这项工作表明，GlyR不仅在脊髓来源的少突胶质细胞中表达，也在上脊髓结构来源的少突胶质细胞中表达。少突胶质细胞GlyR的药理学特性以及推测的分子结构是独特的。在发育中和成熟的少突胶质细胞上存在此类受体的生理意义仍然未知。
