Sodium-dependent, high-affinity taurine transport into rat brain synaptosomes.
Taurine uptake into rat brain synaptosomal fractions appears to occur by two saturable transport processes and by bulk diffusion. The transport requires the presence of sodium ions. The dependence of the transport on temperature and cellular respiration implies that the uptake is an active process. The active process is specific for taurine and closely related amino acids. Brain regions differ in their ability to transport taurine. Uptake is not due to mitochondrial contamination of the synaptosomal fractions. However, glial contamination might partly contribute to the uptake. Kainic acid lesions of rat corpus striatum and cerebellum reduce taurine uptake implying that the uptake is, at least partly, into neurons.
D000818:Animals; D001693:Biological Transport, Active; D001921:Brain / Q000378:metabolism*; D007608:Kainic Acid / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000494:pharmacology; D010101:Oxygen Consumption; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism*; D013654:Taurine / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013696:Temperature
D018377:Neurotransmitter Agents; D013654:Taurine; D012964:Sodium; D007608:Kainic Acid