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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Protein kinase C modulates synaptic vesicle acidification in a ribbon type nerve terminal in the retina.
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Protein kinase C modulates synaptic vesicle acidification in a ribbon type nerve terminal in the retina.

机译：蛋白激酶C调节视网膜带状神经末梢的突触囊泡酸化。

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The driving force for neurotransmitter accumulation into synaptic vesicles is provided by the generation of a transmembrane electrochemical gradient (DeltamuH+) that has two components: a chemical gradient (DeltapH, inside acidic) and an electrical potential across the vesicular membrane (DeltaPsi, inside positive). This gradient is generated in situ by the electrogenic vacuolar H(+)-ATPase, which is responsible for the acidification and positive membrane potential of the vesicle lumen. Here, we investigate the modulation of vesicle acidification by using the acidic-organelle probe LysoTracker and the pH-sensitive probe LysoSensor at goldfish Mb-type bipolar cell terminals. Since phosphorylation can modulate secretory granule acidification in neuroendocrine cells, we investigated if drugs that affect protein kinases modulate LysoTracker staining of bipolar cell terminals. We find that protein kinase C (PKC) activation induces an increase in LysoTracker-fluorescence. By contrast, protein kinase A (PKA) or calcium/calmodulin kinase II (CaMKII) activation or inhibition did not change LysoTracker-fluorescence. Using a pH-dependent fluorescent dye (LysoSensor) we show that the PKC activation with PMA induces an increase in LysoSensor-fluorescence, whereas the inactive analog 4alpha-PMA was unable to cause the same effect. This increase induced by PMA was blocked by PKC inhibitors, calphostin C and staurosporine. These results suggest that phosphorylation by PKC may increase synaptic vesicle acidification in retinal bipolar cells and therefore has the potential to modulate glutamate concentrations inside synaptic vesicles.
机译：跨膜电化学梯度（DeltamuH +）的产生提供了神经递质积聚到突触小泡中的驱动力，该跨膜电化学梯度具有两个成分：化学梯度（DeltapH，在酸性内）和跨囊泡膜的电位（DeltaPsi，在正内）。 。该梯度是由电液泡H（+）-ATPase原位产生的，它负责囊泡内腔的酸化和正膜电位。在这里，我们研究了在金鱼Mb型双极细胞末端使用酸性细胞器探针LysoTracker和pH敏感探针LysoSensor来调节囊泡酸化的过程。由于磷酸化可以调节神经内分泌细胞中分泌性颗粒的酸化，因此我们研究了影响蛋白激酶的药物是否能调节双相细胞末端的LysoTracker染色。我们发现蛋白激酶C（PKC）激活诱导LysoTracker荧光增加。相比之下，蛋白激酶A（PKA）或钙/钙调蛋白激酶II（CaMKII）的激活或抑制作用不会改变LysoTracker荧光。使用pH依赖性荧光染料（LysoSensor），我们显示PMA激活PKC诱导了LysoSensor荧光的增加，而无活性的类似物4alpha-PMA无法引起相同的作用。由PMA诱导的这种增加被PKC抑制剂，钙磷蛋白C和星形孢菌素所阻断。这些结果表明，PKC的磷酸化作用可能会增加视网膜双极细胞中突触小泡的酸化，因此具有调节突触小泡内部谷氨酸浓度的潜力。

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