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UPTAKE AND RELEASE OF <scp>D</scp>‐ AND <scp>L</scp>‐ASPARTATE BY RAT BRAIN SLICES
317
Citations
22
References
1976
Year
High Affinity UptakeSynaptic TransmissionBrain ScienceNeurotransmissionCellular PhysiologySocial SciencesNeurochemistrySodium HomeostasisIon ChannelsNeuropharmacologyGross HyperactivityNervous SystemCerebral Blood FlowPharmacologyPotassium HomeostasisNeurophysiologyCellular NeurosciencePhysiologyNutritional NeuroscienceRapid MetabolismNeuroscienceCentral Nervous SystemMedicine
Abstract— D‐Aspartate is accumulated by slices of adult rat cortex by a high affinity uptake which is abolished if the sodium ions in the incubation medium are replaced by choline. A small uptake of D‐aspartate takes place if the sodium ions are replaced by lithium ions. It appears likely that D‐aspartate shares the same transport system with L‐aspartate, and that the uptake of D‐aspartate is into the same osmotically‐sensitive particles as those which accumulate L‐aspartate. D‐Aspartate is released from cerebral cortex slices by raised potassium concentrations, provided calcium is present in the perfusing buffer. Both D‐ and L‐aspartate produce gross hyperactivity when injected intraperitoneally into immature rats. Radioactive D‐aspartate may be very useful in examining the neurotransmitter role of the naturally‐ occurring L‐aspartate e.g. in studies of the autoradiographic localization of high affinity L‐aspartate accumulation, its main advantage being that, unlike L‐aspartate, D‐aspartate does not undergo rapid metabolism.
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