Zabłocka B, Domańska-Janik K
Department of Neurochemistry, Polish Academy of Sciences, Warsaw.
Acta Neurobiol Exp (Wars). 1993;53(1):25-9.
(1) We favour a hypothesis that the delayed neuronal injury in hippocampus is initiated by the increase of intracellular calcium concentration, activating transiently Ca-dependent protein kinase. (2) The secondary effects of the postischemic, short-lasting PKC translocation/activation could involve: an activation of cAMP signaling pathway; an activation of early response protein like ornitine decarboxylase.
(1) 我们支持这样一种假说，即海马体中延迟性神经元损伤是由细胞内钙浓度升高引发的，它会短暂激活钙依赖性蛋白激酶。(2) 缺血后短暂的蛋白激酶C易位/激活的继发性效应可能包括：环磷酸腺苷信号通路的激活；鸟氨酸脱羧酶等早期反应蛋白的激活。
