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Uptake of γ‐Aminobutyric Acid and Glycine by Synaptosomes from Postmortem Human Brain
Author(s) -
Hardy J. A.,
Barton A.,
Lofdahl E.,
Cheetham S. C.,
Johnston G. A. R.,
Dodd P. R.
Publication year - 1986
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.1471-4159.1986.tb04523.x
Subject(s) - glycine , nipecotic acid , neurochemical , aminobutyric acid , neurotransmitter , biochemistry , synaptosome , chemistry , human brain , amino acid , neurotransmitter transporter , biophysics , biology , neuroscience , in vitro , receptor
Synaptosomes prepared from frozen postmortem human brain accumulated the neurotransmitter γ‐aminobutyric acid (GABA) and the conformationally restricted GABA analogue cis ‐3‐aminocyclohexanecarboxylic acid (ACHC) by a sodium‐dependent, temperature‐sensitive, high‐affinity transport process into an osmotically sensitive compartment. This transport process could be inhibited by GABA analogues (ACHC, 2,4‐di‐aminobutyric acid, nipecotic acid, arecaidine, guvacine) that have been shown in studies on other species to be relatively selective for neuronal rather than glial uptake systems, whereas the glial uptake inhibitor β‐alanine was ineffective. Synaptosomes prepared from frozen postmortem human medulla and spinal cord, but not cerebral cortex, took up the neurotransmitter glycine by a sodium‐dependent high‐affinity transport process. The kinetic parameters for the high‐affinity uptake of GABA, ACHC. and glycine were K m = 10 ± 3, 49 ± 19, and 35 ± 19 μ M; and V max = 98 ± 15, 84 ± 25, and 5.5 ± 2.5 nmol/min/100 mg protein, respectively. These results demonstrate the feasibility of using human CNS preparations for studying GABA and glycine uptake, and suggest that such studies may be useful neurochemical markers for transmitter‐specific presynaptic terminals in health and disease.