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NET UPTAKE OF L‐GLUTAMATE AND GABA BY HIGH AFFINITY SYNAPTOSOMAL TRANSPORT SYSTEMS
Author(s) -
Roskoski Robert
Publication year - 1978
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1978.tb02663.x
Subject(s) - glutamate receptor , synaptosome , chemistry , neurotransmitter , biophysics , biochemistry , reuptake , biology , receptor , serotonin , in vitro
— Reuptake of neuroactive amino acids by high affinity transport systems in the CNS is thought to terminate the neurotransmitter activity of these substances. This notion has been challenged since the homoexchange of synaptosomal and exogenous L‐glutamate and the corresponding homoexchange of synaptosomal and exogenous GABA has been demonstrated. We reported that depolarizing media (56 mM‐KCl, 1 mM‐CaCl 2 ) lowers the GABA content of synaptosomes. In such synaptosomes, net and apparent (radioactive) GABA uptake are similar. When rat cortical synaptosomes (1 mg protein/ml) are incubated with 10μM‐[ 14 C] L‐glutamate, net and apparent (radioactive) uptake are similar. When the synaptosome levels are decreased to 0.5 mg protein/ml or less, then net uptake becomes a fraction of radioactive uptake (exchange ensues). Net L‐glutamate uptake is Na + ‐dependent and temperature‐dependent. Furthermore, a 1 mM concentration of KCl or RbCl supports net L‐glutamate and GABA uptake. LiCl, NH 4 Cl, CsCl and choline chloride are ineffective. In addition, diaminobutyric acid (but not β ‐alanine) inhibits net and apparent GABA uptake. The demonstration of net uptake of L‐glutamate and GABA by their respective high affinity systems is consonant with the idea that these systems may play a role in neurotransmitter inactivation in the synaptic region.

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