Glycine: Inhibition from the Sacrum to the Medulla

Aprison, M. H.; Nadi, N. S.

doi:10.1007/978-1-4613-4030-0_42

Cited by 44 publications

(22 citation statements)

References 130 publications

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“…This uneven distribution of the glycine uptake system is in accord with the high concentration of glycine (2), glycine receptors (35), and the Na+-dependent high-affinity glycine uptake system (37,38) in the spinal cord. Moreover, the differential distribution of these vesicular uptake systems is consistent with the observations that GABA, glycine, and glutamate are accumulated in different populations of nerve endings (9,10,39 …”

mentioning

confidence: 71%

“…y-Aminobutyric acid (GABA) and glycine are the major inhibitory neurotransmitters in the vertebrate central nervous system (1,2). Recently, the primary structures of GABAA and glycine receptors have been deduced; the subunits of these receptors have been shown to have substantial sequence homology, particularly in the region thought to be involved in conducting chloride (3).…”

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confidence: 99%

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Active transport of gamma-aminobutyric acid and glycine into synaptic vesicles.

Kish

Fischer-Bovenkerk

Ueda

1989

Proc. Natl. Acad. Sci. U.S.A.

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Although y-aminobutyric acid (GABA) and glycine are recognized as major amino acid inhibitory neurotransmitters in the central nervous system, their storage is poorly understood. In this study we have characterized vesicular GABA and glycine uptakes in the cerebrum and spinal cord, respectively. We present evidence that GABA and glycine are each taken up into isolated synaptic vesicles in an ATPdependent manner and that the uptake is driven by an electrochemical proton gradient. Uptake for both amino acids exhibited kinetics with low affinity (Km in the millimolar range) similar to vesicular glutamate uptake. The ATP-dependent GABA uptake was not inhibited by the putative amino acid neurotransmitters glycine, taurine, glutamate, or aspartate or by GABA analogs, agonists, and antagonists. Similarly, ATPdependent glycine uptake was hardly affected by GABA, taurine, glutamate, or aspartate or by glycine analogs or antagonists. The GABA uptake was not affected by chloride, which is in contrast to the uptake of the excitatory neurotransmitter glutamate, whereas the glycine uptake was slightly stimulated by low concentrations of chloride. Tissue distribution studies indicate that the vesicular uptake systems for GABA, glycine, and glutamate are distributed in different proportions in the cerebrum and spinal cord. These results suggest that the vesicular uptake systems for GABA, glycine, and glutamate are distinct from each other. y-Aminobutyric acid (GABA) and glycine are the major inhibitory neurotransmitters in the vertebrate central nervous system (1, 2). Recently, the primary structures of GABAA and glycine receptors have been deduced; the subunits of these receptors have been shown to have substantial sequence homology, particularly in the region thought to be involved in conducting chloride (3). GABA and glycine are released upon membrane depolarization, both in a calcium-dependent manner (4-6) and in a calciumindependent manner (4, 7). Recent evidence indicates that the calcium-dependent release of GABA originates from a noncytoplasmic compartment (8). There are also observations indicating that GABA and glycine are concentrated in distinct nerve terminals (9, 10). However, localization of endogenous amino acids in synaptic vesicles has not been clearly demonstrated, either with intact tissues or isolated vesicle preparations. In addition, there has been little study on the vesicular GABA and glycine uptake processes. We have previously provided evidence that glutamate is taken up into synaptic vesicles by a proton-motive force generated by a proton-pump ATPase in the vesicle (11-13). In this communication, we have studied vesicular GABA and glycine uptake, using a synaptic vesicle preparation different from that previously used for vesicular glutamate uptake. We provide evidence that suggests that GABA and glycine are also accumulated into synaptic vesicles in an ATP-dependent manner and that their uptake is driven by an electrochemical proton gradient. We have characterized these uptake systems with r...

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confidence: 71%

mentioning

confidence: 99%

Active transport of gamma-aminobutyric acid and glycine into synaptic vesicles.

Kish

Fischer-Bovenkerk

Ueda

1989

Proc. Natl. Acad. Sci. U.S.A.

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“…It seems most probable that a potentiating effect of Gly and Ser on synaptic transmission in the hippocampus does not occur under physiological conditions, because concentrations of amino acids in the extracellular medium within the brain are only about 1 #M [26 ]. However, a considerable increase in the Gly and Ser concentrations is observed under hypoxic conditions in the brain tissue [7 ]; thus, under these conditions the amino acids may modulate synaptic transmission.…”

Section: Discussionmentioning

confidence: 94%

Glycine and serine as tentative agonists for metabotropic glutamate receptors

et al. 1997

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In experiments on slices of the rat hippocampus, glycine (Gly) and serine (Ser) in concentrations of 100/~M to 1 mM were found to reversibly increase the amplitudes of population EPSP (pEPSP) in pyramidal neurons of the CA1 hippocampal area, evoked by single electrical stimuli applied to Schaffer collaterals (SchC). This potentiation was not affected by 100/zM of a non-competetive antagonist of NMDA glutamate receptors (GR), ketamine, but was considerably weakened by 500 /~M of a competitive antagonist of metabotropic GR (mGR), (• boxyphenylglycine (CFG). The effects of Gly and Ser were not observed in the presence of 50/~M of a blocker of protein kinase C (PKC) catalytic subunit, polymixin B, hut were not modified by preliminary action on the slices of 10 /~M of a calmodulin inhibitor, substance W-7. Gly and Ser also enhanced long-term post-tetanic potentiation (LTPP) of synaptic transmission caused by high-frequency rhythmic stimulation of SchC. Low-frequency (1/sec, 15 rain) SchC stimulation abolished the potentiation of synaptic transmission evoked either by high-frequency SchC stimulation or by the actions of Gly and Set. The data allow us to suggest that Gly and Ser in millimolar concentrations activate mGR, enhance relay functions of the synapses of pyramidal neurons in the CAI hippocampal region, and facilitate plastic modifications in these synapses.

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“…These studies have shown that the cuneate nucleus contains high densities of glycine receptors and glycine-IR neurons. As described previously (Aprison and Nadi, 1978;Lue et al, 1997c;Ottersen et al, 1988), the immunogold-labelled glycine-IR terminals were dotted with numerous gold particles scattering over the cytosol, agranular synaptic vesicles and mitochondria. Present results have further ascertained that the dendrites and somata postsynaptic to the glycine-IR terminals originated from the CTNs.…”

Section: Discussionmentioning

confidence: 99%