RESUMEN
Thymosin fraction five (TF5), a well-characterized immunoregulatory thymic preparation, has been reported to stimulate corticotropin (ACTH) release. The present study explores the morphogenetic role of TF5 on early stages of nerve tissue formation during embryogenesis. In vivo TF5-treatment of newt embryos during neurulation results in stimulation of the process expressed at a macro-microscopical level by emphasizing the embryo's relief and by accelerating the neural tube closure. The stimulating effect of TF5 on neurulation is manifested ultrastructurally by enhanced apical endocytosis, a well-developed contractile microfilamentous layer, increased apical intercellular junctions and changes of the cytoplasmic organelles linked with the protein synthesis. The polymorphism of mitochondria and the morphological expression of enhanced yolk material assimilation confirm the idea of TF5-stimulating effect on the neuroepithelial cells.
Asunto(s)
Embrión no Mamífero/efectos de los fármacos , Sistema Nervioso/efectos de los fármacos , Timosina/análogos & derivados , Animales , Células Epiteliales/efectos de los fármacos , Sistema Nervioso/embriología , Salamandridae , Timosina/farmacologíaRESUMEN
Inhibiting enterocytogenin (IEG), a 4.5 kDa nucleopeptide isolated from pig intestinal mucosa induced dose-dependent alterations in the spontaneous contractile and bioelectric activities of rat gastric smooth muscle when applied at 10(-8) to 10(-4) M. Two separate phases were apparent in the effects observed, an initial contractile phase followed by a relaxation phase. The depolarization and the related contraction were reduced by amiloride and to a lesser extent by nifedipine. This reduction resulted in a corresponding decrease in the magnitude of the subsequent relaxation phase. Charybdotoxin and apamin caused a statistically significant decrease in the hyperpolarization and the magnitude of the relaxation phase and increased the duration of the contractile phase. On a caffeine or noradrenaline background the effects induced by IEG were diminished, suggesting that they are mediated through Ca2+ release from the intracellular Ca2+ stores. We hypothesize that the depolarization induced by IEG involves activation of the voltage-dependent Ca2+ channels with subsequent stimulation of the Ca(2+)-dependent K+ channels and late development of hyperpolarization.