INVIVO BRAIN DIALYSIS STUDY OF THE SOMATODENDRITIC RELEASE OF SEROTONIN IN THE RAPHE NUCLEI OF THE RAT - EFFECTS OF 8-HYDROXY-2-(DI-N-PROPYLAMINO)TETRALIN
INVIVO BRAIN DIALYSIS STUDY OF THE SOMATODENDRITIC RELEASE OF SEROTONIN IN THE RAPHE NUCLEI OF THE RAT - EFFECTS OF 8-HYDROXY-2-(DI-N-PROPYLAMINO)TETRALIN
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DOI：
10.1111/j.1471-4159.1993.tb13390.x
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发表时间：
1993-05-01
影响因子：
4.7
通讯作者：
ARTIGAS, F
中科院分区：
文献类型：
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作者：
ADELL, A;CARCELLER, A;ARTIGAS, F
采用在体微透析技术研究了大鼠中缝背核和中缝正中核5-羟色胺（5-HT）输出的特征。灌注液中加入KCl后，5-HT的基础输出量增加。相反，无论是省略钙离子还是添加0.5 μ M河豚毒素都不会影响透析液5-HT或5-羟基吲哚乙酸（5-HIAA）。利血平没有减少输出的5-HT和5-HIAA 24小时后，对氯苯丙胺增加5-HT在车辆和利血平治疗的大鼠几倍。将1或10 μ M的8-羟基-2-（二正丙基氨基）四氢萘（8-OH-DPAT）灌注到中缝中不改变5-HT或5-HIAA的输出。更高剂量（0. 1，1，和10 mM）增加细胞外5-HT中缝，可能通过抑制摄取。在携带两种探针（中缝核和腹侧海马）的动物中，只有注入中缝核的10 mM剂量的8-OH-DPAT才减少5-HT和5-HIAA的海马输出。全身注射0.1 mg/kg 8-OH-DPAT可降低中缝核和海马中透析液5-HT和5-HIAA的含量。这些结果表明，细胞外5-HT中缝核起源于细胞质池，并不依赖于任何5-HT神经元的神经冲动或5-HT 1A受体的局部激活。
The characteristics of the serotonin (5-HT) output in the dorsal and median raphe nuclei of the rat were studied using in vivo microdialysis. The basal output of 5-HT increased after KCl was added to the perfusion fluid. In contrast, neither the omission of calcium ions nor the addition of 0.5 muM tetrodotoxin affected dialysate 5-HT or 5-hydroxyindoleacetic acid (5-HIAA). Reserpine did not decrease the output of 5-HT and 5-HIAA 24 h later and p-chloroamphetamine increased 5-HT in both vehicle- and reserpine-treated rats severalfold. 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), at 1 or 10 muM, perfused into the raphe did not change the outputs of 5-HT or 5-HIAA. Higher doses (0. 1, 1, and 10 mM) increased extracellular 5-HT in the raphe, probably via an inhibition of uptake. In animals bearing two probes (raphe nuclei and ventral hippocampus), only the 10 mM dose of 8-OH-DPAT perfused into the raphe decreased the hippocampal output of 5-HT and 5-HIAA. The systemic injection of 0.1 mg/kg 8-OH-DPAT decreased dialysate 5-HT and 5-HIAA in the raphe and hippocampus. These results suggest that extracellular 5-HT in raphe nuclei originates from a cytoplasmic pool and is not dependent on either nerve impulse of 5-HT neurons or local activation of 5-HT1A receptors.