Scatton B, Serrano A, Rivot J P, Nishikawa T
Brain Res. 1984 Jul 9;305(2):343-52. doi: 10.1016/0006-8993(84)90440-2.
In vivo differential pulse voltammetry with electrochemically treated carbon fiber microelectrodes has been used to investigate the anatomical nature of the GABAergic influence on striatal serotonergic transmission in the rat. Lesion studies and pharmacological treatments demonstrated that the electrochemical signal recorded at 300 mV in the striatum probably corresponds to the oxidation of extracellularly released 5-hydroxyindoleacetic acid. Thus, dorsal raphé lesions or systemic administration of alpha-propyldopacetamide, NSD 1015, pargyline and MK212 decreased, whereas reserpine injection increased the amplitude of the signal. Moreover, L-5-hydroxytryptophan administration caused an increase in the signal which was almost completely prevented by pargyline pretreatment. Acute administration of dipropylacetamide (150 mg/kg i.p.) reduced the amplitude of the signal from the striatum, while injection of gamma-acetylenic GABA (200 mg/kg i.p.) was without effect. Repeated (but not acute) treatment with the GABA receptor agonist, progabide (400 mg/kg i.p.b.i.d. for 14 days), led to a pronounced decrease in the amplitude of the signal from the striatum. A similar effect was observed after intradorsal raphé infusion of GABA (10 and 100 micrograms), gamma-vinyl GABA (100 micrograms) and SL 75102 (10 micrograms), a principal metabolite of progabide. In contrast, local injection of the GABA receptor antagonists, bicuculline (1 and 10 micrograms) or R5135 (0.05 microgram), failed to affect the peak amplitude in the striatum. When infused into the dorsal raphé, R5135 (0.05-0.1 microgram) antagonized the diminution of the signal induced by intradorsal raphé infusion of GABA (100 micrograms) or SL 75102 (10 micrograms). Finally, electrolytic lesion of the habenular nuclei completely blocked the diminution of the signal from striatum induced by an intradorsal raphé infusion of GABA (100 micrograms). These results indicate that the inhibitory GABAergic control of striatal serotonergic transmission is exerted at the level of the dorsal raphé cells and depends upon the integrity of the habenulo-dorsal pathway.
采用经电化学处理的碳纤维微电极进行体内差分脉冲伏安法，以研究大鼠纹状体中γ-氨基丁酸能对5-羟色胺能传递的解剖学影响。损伤研究和药物治疗表明，在纹状体中300 mV记录的电化学信号可能对应于细胞外释放的5-羟吲哚乙酸的氧化。因此，背侧中缝核损伤或全身给予α-丙基多巴酰胺、NSD 1015、帕吉林和MK212可使信号幅度降低，而注射利血平则增加信号幅度。此外，给予L-5-羟色氨酸可使信号增加，而帕吉林预处理几乎可完全阻止这种增加。急性给予二丙基乙酰胺（150 mg/kg腹腔注射）可降低纹状体信号幅度，而注射γ-炔丙基氨基丁酸（200 mg/kg腹腔注射）则无作用。重复（而非急性）给予γ-氨基丁酸受体激动剂普罗加比（400 mg/kg腹腔注射，每日两次，共14天）可导致纹状体信号幅度显著降低。在背侧中缝核内注入γ-氨基丁酸（10和100微克）、γ-乙烯基氨基丁酸（100微克）和普罗加比的主要代谢产物SL 75102（10微克）后也观察到类似效果。相反，局部注射γ-氨基丁酸受体拮抗剂荷包牡丹碱（1和10微克）或R5135（0.05微克）未能影响纹状体中的峰值幅度。当注入背侧中缝核时，R5135（0.05 - 0.1微克）可拮抗背侧中缝核内注入γ-氨基丁酸（100微克）或SL 75102（10微克）所诱导的信号减弱。最后，缰核电解损伤可完全阻断背侧中缝核内注入γ-氨基丁酸（100微克）所诱导的纹状体信号减弱。这些结果表明，纹状体5-羟色胺能传递的抑制性γ-氨基丁酸能控制作用于背侧中缝核细胞水平，并依赖于缰核-背侧通路的完整性。
