RELEASE OF ASCORBATE FROM A SYNAPTOSOMAL FRACTION OF RAT-BRAIN
RELEASE OF ASCORBATE FROM A SYNAPTOSOMAL FRACTION OF RAT-BRAIN
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DOI：
10.1016/0197-0186(84)90120-7
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发表时间：
1984-01-01
影响因子：
4.2
通讯作者：
FILLENZ, M
中科院分区：
文献类型：
--
作者：
GRUNEWALD, RA;FILLENZ, M
本文研究了控制大鼠脑不同区域突触体内源性抗坏血酸释放的因素。抗坏血酸从突触体自发释放，这种流出可通过在37 ℃孵育来增强。C.一个进一步的额外的抗坏血酸释放可以诱导：K去极化或在纹状体，海马和皮质突触体或孵育的氨基酸谷氨酸。自发去极化和谷氨酸诱发的抗坏血酸释放被证明是通过不同的机制发生的。谷氨酸引起的抗坏血酸释放发生的异交换机制。在小脑突触体中，没有证据表明存在这种异交换;然而，在该大脑区域的突触体中，红藻氨酸可能通过作用于兴奋性氨基酸受体来诱导抗坏血酸的释放。结果进行了讨论，在细胞外的脑抗坏血酸发生在体内的变化。
Factors controlling the release of endogenous ascorbate from synaptosomes prepared from various regions of the rat brain was studied. Ascorbate was spontaneously released from synaptosomes, and this efflux could be enhanced by incubation at 37.degree. C. A further additional ascorbate release could be induced by: K depolarization or in striatal, hippocampal, and cortical synaptosomes or by incubation with the amino acid glutamate. Spontaneous depolarization and glutamate-evoked ascorbate release was shown to occur by separate mechanisms. Glutamate-evoked ascorbate release occurred by a heteroexchange mechanism. In cerebellar synaptosomes there was no evidence for such heteroexchange; however, in synaptosomes of this brain region kainic acid induced ascorbate release, probably by acting on excitatory amino acid receptors. The results are discussed in relation to the changes in extracellular brain ascorbate occurring in vivo.