Miyauchi T, Kitada Y, Nakamichi H, Satoh S
Life Sci. 1984 Jul 30;35(5):543-51. doi: 10.1016/0024-3205(84)90248-0.
The immobility-reducing action of desipramine (DMI) in forced swimming rats was attenuated by intracerebroventricular (i.c.v.) injection of isoproterenol (ISO) and potentiated by i.c.v. atenolol (ATE), a beta 1-adrenoceptor antagonist. The effect of ISO was blocked by ATE. When administered i.c.v. in normal rats, ISO reduced the contents of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), a major metabolite of noradrenaline, in the septal area, thalamus and hypothalamus while ATE had no effect in most of the brain regions. However, in forced swimming rats treated with DMI, ISO reduced MHPG-SO4 in 6 out of 8 brain regions tested and conversely, ATE increased the levels in the amygdala, septal area and hypothalamus. Similar to the behavioral effect, the effect of ISO was antagonized by ATE. These results support the hypothesis that central beta 1-adrenergic mechanisms inhibit the immobility-reducing action of DMI by reducing the activity of noradrenergic neurons in the brain.
在强迫游泳的大鼠中，地昔帕明（DMI）的减少不动行为的作用，通过脑室内（i.c.v.）注射异丙肾上腺素（ISO）而减弱，并因脑室内用药阿替洛尔（ATE，一种β1 -肾上腺素能受体拮抗剂）而增强。ISO的作用被ATE阻断。当在正常大鼠中进行脑室内给药时，ISO降低了隔区、丘脑和下丘脑（去甲肾上腺素的主要代谢产物3 -甲氧基 - 4 -羟基苯乙二醇硫酸盐（MHPG - SO4））的含量，而ATE在大多数脑区没有影响。然而，在用DMI治疗的强迫游泳大鼠中，ISO在8个测试脑区中的6个降低了MHPG - SO4，相反，ATE增加了杏仁核、隔区和下丘脑的水平。与行为效应相似，ISO的作用被ATE拮抗。这些结果支持这样的假说，即中枢β1 -肾上腺素能机制通过降低脑中去甲肾上腺素能神经元的活性来抑制DMI减少不动行为的作用。
