O'Neill R D, Fillenz M, Grünewald R A, Bloomfield M R, Albery W J, Jamieson C M, Williams J H, Gray J A
Neurosci Lett. 1984 Mar 9;45(1):39-46. doi: 10.1016/0304-3940(84)90326-4.
Changes in the height of peak 2 obtained using linear sweep voltammetry and carbon paste electrodes chronically implanted in discrete brain regions of the unrestrained rat were measured under a variety of conditions; in the past this peak has been attributed to the oxidation of 5-hydroxyindoleacetic acid (5-HIAA). Unilateral 5,7-dihydroxytryptamine (5,7-DHT) lesions of the medial forebrain bundle reduced the 5-HIAA content of the striatum and hippocampus to 10% of the unlesioned side, but did not alter the height of peak 2 recorded in these regions. In contrast, microinfusion of uricase beside striatial electrodes reduced the height of peak 2 by 96%; systemic amphetamine-induced increases in the height of the peak were also prevented by this enzyme. These results indicate that uric acid, and not 5-HIAA, is mainly responsible for peak 2, and that changes in the height of this peak reflect changes in the extracellular concentration of uric acid.
使用线性扫描伏安法和长期植入未束缚大鼠离散脑区的碳糊电极，在多种条件下测量了峰2高度的变化；过去该峰被认为归因于5-羟吲哚乙酸（5-HIAA）的氧化。内侧前脑束的单侧5,7-二羟基色胺（5,7-DHT）损伤使纹状体和海马体的5-HIAA含量降至未损伤侧的10%，但并未改变这些区域记录的峰2高度。相比之下，在纹状体电极旁微量注入尿酸酶使峰2高度降低了96%；该酶也阻止了全身注射苯丙胺引起的峰高增加。这些结果表明，主要是尿酸而非5-HIAA导致峰2出现，且该峰高度的变化反映了细胞外尿酸浓度的变化。
