Incubation of cultured neurons from chick embryo forebrain with corticotropin (ACTH) or the phorbol ester TPA (12-O-tetradecanoylphorbol 13-acetate) stimulates the production of lactate. The stimulation is seen after 2 h of treatment and is maximal after 12 h. Both ACTH (1-24) and TPA increase the concentration of fructose 2,6-bisphosphate (Fru-2,6-P2), a metabolic activator of 6-phosphofructo-1-kinase (PFK-1). This effect is concentration-dependent and is maximal after 4 h of treatment. PFK-1 activity is increased in a dose-dependent manner by ACTH (1-24) or TPA. This increase is not visible during the first 6 h and reaches its maximum after 8 h of treatment. The stimulation of PFK-1 activity is not due the increase of Fru-2,6-P2by ACTH (1-24) or TPA, since saturating concentrations of Fru-2,6-P2are present in the PFK-1 assay medium. Thus, it appears that ACTh (1-24) and TPA regulate glycolysis through two modes with different time responses: increase in Fru-2,6-P2is the main mechanism operating during the first 6 h following the treatments and increase in the amount, or stable increase in activity of PFK-1, takes place during the later phase. It is suggested that the action of corticotropin on glycolysis is part of the mechanism of the neurotrophic activity of this hormone. © 1992.
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