Price Gareth D, Trussell Laurence O
Oregon Hearing Research Center, Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.
J Neurosci. 2006 Nov 1;26(44):11432-6. doi: 10.1523/JNEUROSCI.1660-06.2006.
The function of presynaptic terminals is regulated by intracellular Cl-, the levels of which modify vesicular endocytosis and transmitter refilling and mediate the effects of presynaptic ligand-gated Cl- channels. Nevertheless, the concentration of Cl- in a central nerve terminal is unknown, and it is unclear whether terminals can regulate Cl- independently of the soma. Using perforated-patch recording in a mammalian synapse, we found that terminals accumulate Cl- up to 21 mm, between four and five times higher than in their parent cell bodies. Changing [Cl-] did not alter vesicular glutamate content in intact terminals, unlike in vitro experiments. Thus, glutamatergic terminals maintain an elevated Cl- concentration without compromising synaptic transmission.
突触前终末的功能受细胞内氯离子调控，其水平会改变囊泡内吞作用和递质再填充，并介导突触前配体门控氯离子通道的效应。然而，中枢神经终末内氯离子的浓度尚不清楚，而且终末是否能独立于胞体调节氯离子也不明确。通过在哺乳动物突触中进行穿孔膜片钳记录，我们发现终末积累的氯离子高达21 mM，比其母细胞体中的氯离子浓度高四到五倍。与体外实验不同，改变[Cl-]并不会改变完整终末内囊泡谷氨酸的含量。因此，谷氨酸能终末维持着较高的氯离子浓度，而不会损害突触传递。
