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大鼠脑突触体组分中抗坏血酸的释放。

Release of ascorbate from a synaptosomal fraction of rat brain.

作者信息

Grünewald R A, Fillenz M

机构信息

University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, U.K.

出版信息

Neurochem Int. 1984;6(4):491-500. doi: 10.1016/0197-0186(84)90120-7.

Abstract

We have studied factors controlling the release of endogenous ascorbate from synaptosomes prepared from various regions of the rat brain. Ascorbate was spontaneously released from synaptosomes, and this efflux could be enhanced by incubation at 37 degrees C. A further additional ascorbate release could be induced by potassium depolarization or, in striatal, hippocampal and cortical synaptosomes, by incubation with the amino acid glutamate. Spontaneous, depolarization and glutamate-evoked ascorbate release were 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.

摘要

我们研究了控制从大鼠脑不同区域制备的突触体中内源性抗坏血酸释放的因素。抗坏血酸从突触体中自发释放,并且在37℃孵育可增强这种流出。钾去极化可诱导进一步的额外抗坏血酸释放,或者在纹状体、海马体和皮质突触体中,通过与氨基酸谷氨酸孵育来诱导释放。自发、去极化和谷氨酸诱发的抗坏血酸释放显示是通过不同机制发生的。谷氨酸诱发的抗坏血酸释放通过异质交换机制发生。在小脑突触体中,没有证据表明存在这种异质交换;然而,在该脑区的突触体中, kainic酸诱导抗坏血酸释放,可能是通过作用于兴奋性氨基酸受体。结合体内发生的细胞外脑抗坏血酸变化对结果进行了讨论。

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