Breitinger Ulrike, Breitinger Hans-Georg
Department of Biochemistry, The German University in Cairo, Main Entrance of Al Tagamoa Al Khames, New Cairo 11835, Egypt.
Department of Biochemistry, The German University in Cairo, Main Entrance of Al Tagamoa Al Khames, New Cairo 11835, Egypt.
Neurosci Lett. 2016 Jan 26;612:110-115. doi: 10.1016/j.neulet.2015.11.051. Epub 2015 Dec 2.
The inhibitory glycine receptor (GlyR) mediates rapid synaptic inhibition in the mammalian central nervous system. Recently, glucose was identified as a positive modulator of α1 GlyRs. Here, recombinant human α3GlyRs with and without glucose treatment were studied using patch clamp methods. Similar to α1GlyRs, receptor variants α3L and α3K were potentiated by sugar. Glucose treatment reduced EC50 values of GlyR α3L and α3K by a factor of 4.5 and 3.3, respectively, without affecting maximum currents or desensitization. The high-activity mutant α3L(P185L) was not further potentiated by glucose. Potentiation of glycinergic signalling may underlie some of the analgetic effects of glucose.
抑制性甘氨酸受体（GlyR）介导哺乳动物中枢神经系统中的快速突触抑制。最近，葡萄糖被鉴定为α1甘氨酸受体的正向调节剂。在此，使用膜片钳方法研究了经葡萄糖处理和未经葡萄糖处理的重组人α3甘氨酸受体。与α1甘氨酸受体类似，受体变体α3L和α3K被糖增强。葡萄糖处理分别使甘氨酸受体α3L和α3K的EC50值降低了4.5倍和3.3倍，而不影响最大电流或脱敏。高活性突变体α3L（P185L）未被葡萄糖进一步增强。甘氨酸能信号的增强可能是葡萄糖某些镇痛作用的基础。
