Rapallino M V, Cupello A, Hydén H
Centro di Neurofisiologia Cerebrale, CNR, Genova, Italy.
Neurochem Res. 1999 Aug;24(8):1089-92. doi: 10.1023/a:1021073230464.
The modulation of intracellular GABA activated 36Cl- in-->out permeation across single Deiters' neuron membranes has been studied in a microchamber system. Addition of Mg2+/ATP on the membrane cytoplasmic side reduces strongly the GABA effect as does ATP alone. However, the greatest inhibition of the GABA effect is given by the addition of Mg2+ to the intracellular side buffer: a complete block of the stimulation by GABA of 36Cl- in-->out permeation. This is interpreted as due to the presence in this case of a constant concentration of exogenous Mg2+ acting together with endogenous ATP in the small cytoplasmic layer on the membrane inner side. The addition of ADP to Mg2+/ATP increases the inhibitory effect of the latter. This is presumably due to an extra increase of ATP, locally under the membrane, due to phosphorylation of ADP by endogenous phosphocreatine. Overall, the data confirm that phosphorylating conditions impair the intracellular GABA action on 36Cl- in-->out permeation.
在微腔系统中研究了细胞内γ-氨基丁酸(GABA)对单个Deiters神经元膜上36Cl-外向渗透的调节作用。在膜细胞质侧添加Mg2+/ATP会强烈降低GABA的作用,单独添加ATP时也是如此。然而,在细胞内侧缓冲液中添加Mg2+对GABA作用的抑制作用最大:完全阻断GABA对36Cl-外向渗透的刺激。这被解释为在这种情况下,外源Mg2+的恒定浓度与膜内侧小细胞质层中的内源性ATP共同作用。向Mg2+/ATP中添加ADP会增强后者的抑制作用。这可能是由于内源性磷酸肌酸将ADP磷酸化,导致膜下局部ATP额外增加。总体而言,数据证实磷酸化条件会损害细胞内GABA对36Cl-外向渗透的作用。