Uptake of γ‐Aminobutyric Acid by a Synaptic Vesicle Fraction Isolated from Rat Brain

Fykse, Else Marie; Fonnum, Frode

doi:10.1111/j.1471-4159.1988.tb10599.x

Cited by 126 publications

(69 citation statements)

References 30 publications

(21 reference statements)

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“…6, 19 and 24). This indicates that in the membrane vesicle preparation we have used, the sodiumindependent GABA transporter from the synaptic vesicles (25,26) is below detectable levels. The two subtypes appear to differ only in their substrate binding site.…”

Section: Discussionmentioning

confidence: 98%

Two pharmacologically distinct sodium- and chloride-coupled high-affinity gamma-aminobutyric acid transporters are present in plasma membrane vesicles and reconstituted preparations from rat brain.

Kanner

Bendahan

1990

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

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Section: Discussionmentioning

confidence: 98%

Two pharmacologically distinct sodium- and chloride-coupled high-affinity gamma-aminobutyric acid transporters are present in plasma membrane vesicles and reconstituted preparations from rat brain.

Kanner

Bendahan

1990

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

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“…To check for possibly selective cross-reactivity of the antibodies with synaptic vesicle components, rat brain tissue was fractionated according to Whittaker et al (1964) with modifications as described by Fykse and Fonnum (1988). Fractions of lysed synaptosomes, synaptic vesicles, mitochondria, and cytosol, as well as the nonsynaptosomal cytosolic supernatant from whole brain were tested.…”

Section: Methodsmentioning

confidence: 99%

Synaptic Vesicular Localization and Exocytosis ofl-Aspartate in Excitatory Nerve Terminals: A Quantitative Immunogold Analysis in Rat Hippocampus

et al. 1998

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To elucidate the role of aspartate as a signal molecule in the brain, its localization and those of related amino acids were examined by light and electron microscopic quantitative immunocytochemistry using antibodies specifically recognizing the aldehyde-fixed amino acids. Rat hippocampal slices were incubated at physiological and depolarizing [K ϩ ] before glutaraldehyde fixation. At normal [K ϩ ], aspartate-like and glutamatelike immunoreactivities were colocalized in nerve terminals forming asymmetrical synapses on spines in stratum radiatum of CA1 and the inner molecular layer of fascia dentata (i.e., excitatory afferents from CA3 and hilus, respectively). During K ϩ depolarization there was a loss of aspartate and glutamate from these terminals. Simultaneously the immunoreactivities strongly increased in glial cells. These changes were Ca 2ϩ -dependent and tetanus toxin-sensitive and did not comprise taurine-like immunoreactivity. Adding glutamine at CSF concentration prevented the loss of aspartate and glutamate and revealed an enhancement of aspartate in the terminals at moderate depolarization.In hippocampi from animals perfused with glutaraldehyde during insulin-induced hypoglycemia (to combine a strong aspartate signal with good ultrastructure) aspartate was colocalized with glutamate in excitatory terminals in stratum radiatum of CA1. The synaptic vesicle-to-cytoplasmic matrix ratios of immunogold particle density were similar for aspartate and glutamate, significantly higher than those observed for glutamine or taurine. Similar results were obtained in normoglycemic animals, although the nerve terminal contents of aspartate were lower. The results indicate that aspartate can be concentrated in synaptic vesicles and subject to sustained exocytotic release from the same nerve endings that contain and release glutamate.

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“…Synaptic vesicles were isolated from rat brains as described [34,35]. Two whole brains were homogenized (10% wt./ vol.)…”

Section: Synaptic Vesicles Preparationmentioning

confidence: 99%

Quinolinic Acid-induced Seizures Stimulate Glutamate Uptake into Synaptic Vesicles from Rat Brain: Effects Prevented by Guanine-based Purines

et al. 2007

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Glutamate uptake into synaptic vesicles is a vital step for glutamatergic neurotransmission. Quinolinic acid (QA) is an endogenous glutamate analog that may be involved in the etiology of epilepsy and is related to disturbances on glutamate release and uptake. Guanine-based purines (GBPs) guanosine 5'-monophosphate (GMP and guanosine) have been shown to exert anticonvulsant effects against QA-induced seizures. The aims of this study were to investigate the effects of in vivo administration of several convulsant agents on glutamate uptake into synaptic vesicles and investigate the role of MK-801, guanosine or GMP (anticonvulsants) on glutamate uptake into synaptic vesicles from rats presenting QA-induced seizures. Animals were treated with vehicle (saline 0.9%), QA 239.2 nmoles, kainate 30 mg/kg, picrotoxin 6 mg/kg, PTZ (pentylenetetrazole) 60 mg/kg, caffeine 150 mg/kg or MES (maximal transcorneal electroshock) 80 mA. All convulsant agents induced seizures in 80-100% of animals, but only QA stimulated glutamate uptake into synaptic vesicle. Guanosine or GMP prevented seizures induced by QA (up to 52% of protection), an effect similar to the NMDA antagonist MK-801 (60% of protection). Both GBPs and MK-801 prevented QA-induced glutamate uptake stimulation. This study provided additional evidence on the role of QA and GBPs on glutamatergic system in rat brain, and point to new perspectives on seizures treatment.

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Uptake of γ‐Aminobutyric Acid by a Synaptic Vesicle Fraction Isolated from Rat Brain

Cited by 126 publications

References 30 publications

Two pharmacologically distinct sodium- and chloride-coupled high-affinity gamma-aminobutyric acid transporters are present in plasma membrane vesicles and reconstituted preparations from rat brain.

Two pharmacologically distinct sodium- and chloride-coupled high-affinity gamma-aminobutyric acid transporters are present in plasma membrane vesicles and reconstituted preparations from rat brain.

Synaptic Vesicular Localization and Exocytosis ofl-Aspartate in Excitatory Nerve Terminals: A Quantitative Immunogold Analysis in Rat Hippocampus

Quinolinic Acid-induced Seizures Stimulate Glutamate Uptake into Synaptic Vesicles from Rat Brain: Effects Prevented by Guanine-based Purines

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