Vatta Marcelo, Peña Clara, Fernández Belisario E, Rodríguez de Lores Arnaiz Georgina
Cátedra de Fisiología-IQUIMEFA, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, 1113-Buenos Aires, Argentina.
Life Sci. 2004 Dec 10;76(4):359-65. doi: 10.1016/j.lfs.2004.09.004.
The ability of an endogenous brain Na+, K+ -ATPase inhibitor, termed endobain E, to increase [3H]norepinephrine release in rat hypothalamus was previously reported. Endobain E effect on neurotransmitter uptake was studied by assaying [3H]norepinephrine uptake in rat hypothalamus preparations, to observe uptake inhibition, which reached 60% with endobain E equivalent to 100 mg fresh cerebral cortex, an effect achieved with 40 or 400 microM ouabain. Results support the proposal that endobain E behaves as an ouabain-like substance. Taken jointly results obtained on neurotransmitter release and uptake, the suggestion that endobain E may enhance norepinephrine availability in the synaptic gap and thus lead to an increase in noradrenergic activity is advanced.
先前有报道称,一种内源性脑钠钾ATP酶抑制剂(称为内源性脑钠素E)能够增加大鼠下丘脑[3H]去甲肾上腺素的释放。通过测定大鼠下丘脑制剂中[3H]去甲肾上腺素的摄取来研究内源性脑钠素E对神经递质摄取的影响,以观察摄取抑制情况,当内源性脑钠素E相当于100毫克新鲜大脑皮层时,摄取抑制率达到60%,40或400微摩尔哇巴因也能达到这一效果。结果支持了内源性脑钠素E表现为类似哇巴因物质的提议。综合关于神经递质释放和摄取所获得的结果,提出了内源性脑钠素E可能会提高突触间隙中去甲肾上腺素的可用性,从而导致去甲肾上腺素能活性增加的观点。