Abstract

The release of glycine from slices of the brain stem and binding of strychnine to brain stem membranes were characterized in adult and developing mice. Spontaneous glycine efflux was markedly facilitated by homoexchange with exogenous glycine and moderately by heteroexchange with taurine. Potassium stimulation released more glycine from brain stem slices from adult than from 7-day-old mice. Potassium-stimulated glycine release was also potentiated by glycine and by the novel anticonvulsant taurine derivatives. One population of strychnine-binding sites was found in both mature and immature brain stem. The number of binding sites increased with age, whereas the affinity of the sites for strychnine remained the same. The glycine inhibition was stronger in adult than in developing mice. In the presence of taurine the affinity for strychnine decreased without any change in the maximal binding capacity, suggesting a competitive type of inhibition. The binding constant and maximal binding capacity of strychnine increased in the presence of NaCl (200 mM) both in adult and 7-day-old mice. The calculated IC50 values for displacement of strychnine binding by glycine, taurine and β-alanine were higher in the presence than in the absence of sodium. The results show that the evoked release of glycine and the number of binding sites of strychnine increase during postnatal development in the mouse but that their characteristics do not change.

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