首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Inhibition of catecholamine synthesis with alpha-methyl-p-tyrosine apparently increases brain serotoninergic activity in the rat: no influence of previous chronic immobilization stress.
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Inhibition of catecholamine synthesis with alpha-methyl-p-tyrosine apparently increases brain serotoninergic activity in the rat: no influence of previous chronic immobilization stress.

机译:用α-甲基-对-酪氨酸抑制儿茶酚胺的合成显然会增加大鼠的脑5-羟色胺能活性:不会影响先前的慢性固定应激。

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The functional relationship between brain catecholamines and serotoninergic function was studied in stress-naive and chronically immobilized rats after blockade of catecholamine synthesis with alpha-methyl-p-tyrosine (alpha MpT). The levels of noradrenaline (NA), serotonin, and 5-hydroxyindole acetic acid (5-HIAA) in pons plus medulla, brainstem, hypothalamus, hippocampus, and frontal cortex, and those of 3-methoxy, 4-hydroxyphenile-tileneglicol sulphate (MHPG-SO4) in the hypothalamus were measured by HPLC. Chronic immobilization (IMO) resulted in higher NA levels in pons plus medulla and hypothalamus, the latter area (the only one in which the NA metabolite was determined) also showing slightly elevated MHPG-SO4 levels as compared to stress-naive rats. Chronic IMO did not alter either serotonin or 5-HIAA levels, but acute stress consistently increased 5-HIAA levels in all areas, independently of previous chronic stress. Administration of alpha-MpT drastically reduced NA and increased 5-HIAA levels in all brain regions excepting the frontal cortex. The effect of the drug on serotoninergic function was not altered by previous chronic exposure to IMO. These data suggest that the noradrenergic system appears to exert a tonic inhibitory effect on serotoninergic activity in the brain, with the intensity of the effect depending on the brain area studied. In addition, chronic stress does not appear to alter the functional relationship between noradrenergic and serotoninergic activities, although interactions might exist in more restricted brain areas; this deserves further study.
机译:在用α-甲基-对-酪氨酸(αMpT)阻断儿茶酚胺合成后,在未接受过应激和长期固定的大鼠中研究了儿茶酚胺与5-羟色胺能功能之间的功能关系。脑桥,延髓,脑干,下丘脑,海马和额叶皮层中去甲肾上腺素(NA),5-羟色胺和5-羟吲哚乙酸(5-HIAA)的水平以及3-甲氧基,4-羟苯并-tileneglicol硫酸盐的水平(通过HPLC测量下丘脑中的MHPG-SO 4。慢性固定(IMO)导致脑桥加上延髓和下丘脑的NA水平升高,与未接受过应激的大鼠相比,后者(唯一确定NA代谢产物的区域)的MHPG-SO4水平也略有升高。慢性IMO并没有改变5-羟色胺或5-HIAA的水平,但急性应激在所有区域均持续增加5-HIAA的水平,与先前的慢性应激无关。在额叶皮层以外的所有大脑区域中,α-MpT的施用可大大降低NA,并提高5-HIAA水平。先前对IMO的长期暴露并未改变药物对5-羟色胺能功能的影响。这些数据表明,去甲肾上腺素能系统似乎对大脑中的5-羟色胺能活性具有强直抑制作用,其强度取决于所研究的大脑区域。此外,慢性应激似乎并未改变去甲肾上腺素能与5-羟色胺能活动之间的功能关系,尽管相互作用可能存在于更受限的大脑区域。这值得进一步研究。

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