Goldstein R, Rodica B
Institute of Endocrinology, Bucharest, Romania.
Int J Dev Neurosci. 1986;4(4):305-9. doi: 10.1016/0736-5748(86)90047-x.
Active sleep, brain weight as well as total lipids and galactolipids were assayed in 8-day-old rat pups, after daily administration (between 2 and 8 days of postnatal age) of saline, arginine vasotocin (AVT) (10(-7) mg), picrotoxin (5 x 10(-5) mg), valproic acid (10(-5) and 10(-6) mg) or of AVT + picrotoxin and AVT + valproic acid. AVT increases active sleep and decreases the weight, total lipids and the galactolipids of the brain. Although picrotoxin alone was without any apparent effects on maturational parameters, when administered together with AVT, it completely prevented AVT from producing its effects. Valproic acid had AVT-like effects when administered in a higher dose (10(-5) mg), but was without any apparent effects when administered in the lower dose (10(-6) mg). However, both doses intensely potentiated the effects of AVT. Since both drugs specifically interfere with the GABAergic neurotransmission, it is concluded that AVT retards the accumulation of brain lipids by activating a GABAergic pathway.
在出生后第2至8天每日给8日龄幼鼠注射生理盐水、精氨酸加压催产素(AVT,10⁻⁷毫克)、印防己毒素(5×10⁻⁵毫克)、丙戊酸(10⁻⁵和10⁻⁶毫克)或AVT与印防己毒素及AVT与丙戊酸的组合后,对其主动睡眠、脑重量以及总脂质和半乳糖脂进行了测定。AVT增加主动睡眠并降低脑重量、总脂质和半乳糖脂。虽然单独使用印防己毒素对成熟参数没有任何明显影响,但与AVT一起给药时,它完全阻止了AVT产生其作用。丙戊酸在较高剂量(10⁻⁵毫克)给药时具有类似AVT的作用,但在较低剂量(10⁻⁶毫克)给药时没有任何明显影响。然而,两种剂量都强烈增强了AVT的作用。由于这两种药物都特异性地干扰GABA能神经传递,因此得出结论,AVT通过激活GABA能途径延缓脑脂质的积累。