Transport of histidine into synaptosomes of the rat central nervous system.
Histidine transport into synaptosomes was studied in order to characterize this aspect of histamine synthesis in neurons. Histidine transport was found to be independent of sodium, calcium, and magnesium ions and dependent upon potassium and chloride ions. Histidine transport was also found to be energy dependent, and fractionation studies suggested it was highly localized to nerve terminals. Kinetic analysis of histidine transport in several brain regions indicated the presence of two uptake sites, a high-affinity site with a Km of approximately 35 microM and a low-affinity site with a Km in the millimolar range. Density of the high-affinity site, as reflected by Vmax, correlates well with density of proposed histaminergic innervation. Rate of histidine transport was not altered by prior depolarization of the synaptosomes, indicating that histidine transport probably does not play a regulatory role in histamine synthesis.
D019297:2,4-Dinitrophenol; D000818:Animals; D001693:Biological Transport, Active; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D004140:Dinitrophenols / Q000494:pharmacology; D006639:Histidine / Q000378:metabolism*; D008274:Magnesium / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000494:pharmacology; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*
D004140:Dinitrophenols; D006639:Histidine; D011189:Potassium Chloride; D012964:Sodium; D008274:Magnesium; D019297:2,4-Dinitrophenol