Krivánek J
Physiol Bohemoslov. 1984;33(1):23-30.
Pretreatment of the rat cerebral cortex by topical application of 1.5 mol X 1(-1) MgCl2 in order to prevent the induction of spreading depression by depolarizing agents did not inhibit but potentiated the ability of 1.0 mol X 1(-1) K+ (39 pmol cAMP/mg prot.) and 0.2 mol X 1(-1) veratridine [11 pmol cAMP/mg prot.] to produce the accumulation of cyclic adenosine monophosphate [cAMP] by 110% and 180% respectively. Hypertonic NaCl solutions [2.0 and 3.5 mol X 1(-1)] alone did not affect the normal cAMP levels in the cortex, neither was the effect of K+ modulated by pretreatment of the cortex by topical application of 3.5 mol X 1(-1) NaCl. Additive effects of K+ and veratridine were found on cAMP formation. The mechanism of potassium-stimulation of cAMP formation and the effect of Mg2+ is discussed.
通过局部应用1.5 mol·L⁻¹MgCl₂对大鼠大脑皮层进行预处理，以防止去极化剂诱导扩散性抑制，结果并未抑制反而增强了1.0 mol·L⁻¹K⁺（39 pmol cAMP/mg蛋白）和0.2 mol·L⁻¹藜芦定[11 pmol cAMP/mg蛋白]使环磷酸腺苷[cAMP]积累的能力，分别增加了110%和180%。单独的高渗NaCl溶液[2.0和3.5 mol·L⁻¹]不影响皮层中的正常cAMP水平，通过局部应用3.5 mol·L⁻¹NaCl对皮层进行预处理也不会调节K⁺的作用。发现K⁺和藜芦定对cAMP形成具有相加作用。文中讨论了钾刺激cAMP形成的机制以及Mg²⁺的作用。
