Calcium dependent release of γ-aminobutyric acid (GABA) from human cerebral cortex

Haugstad, Tor S.; Hegstad, Elisabeth; Langmoen, Iver A.

doi:10.1016/0304-3940(92)90334-4

Cited by 19 publications

(7 citation statements)

References 22 publications

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“…Synaptic transmission depends on the presence of extracellular Ca ++ [26] and studies on experimental animals have shown that calcium deprivation combined with elevated magnesium in the incubation fluid reliably block synaptic release and transmission [2]. In agreement with this we found that both glutamate and GABA were released from human slices in a Ca++-dependent manner during potassium induced depolarization [20,21]. In contrast, the total release of several amino-acids, including glutamate and GABA, during 20 min of ED was not affected by conditions blocking synaptic release.…”

Section: Discussionsupporting

confidence: 81%

“…Peak release of aspartate, glycine and GABA was 25, 154, and 35 pmol/mg/min, respectively. In Ca++-ffee incubation fluid [20,21] the release of GABA and glutamate, but not aspartate and glycine, was reduced by 50 and 66%, respectively.…”

Section: Amino-acid Release Induced By Depolarizationmentioning

confidence: 93%

“…Both glutamate and GABA fulfill criteria for putative neurotransmitters in human brain, regarding presence in presynaptic terminals, Ca++-dependent release and high-affinity uptake [1,14,20,21,46].…”

Section: Introductionmentioning

confidence: 99%

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Amino-acid release from human cerebral cortex during simulated ischaemia in vitro

Hegstad

Berg-Johnsen

et al. 1996

Acta neurochir

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The aim of the present study was to investigate the release of amino-acids in human cerebral cortex during membrane depolarization and simulated ischaemia (energy deprivation). Superfluous tissue from temporal Iobe resections for epilepsy was cut into 500 microns thick slices and incubated in vitro. Membrane depolarization with 50 mM K+ caused a release of glutamate, aspartate, GABA and glycine, but not glutamine or leucine. The release of glutamate and GABA was Ca(++)-dependent. Slices were exposed to simulated ischaemia (energy deprivation; ED) by combined glucose/oxygen deprivation. This caused a Ca(++)-independent release of glutamate, aspartate, GABA, glycine, and taurine which started after 8 min, peaked at the end or shortly after the 27 min period of ED, and returned to control levels within 11 min following termination of ED. Preloaded D-[3H]aspartate was released both during K(+)-stimulation and ED. Release of D-[3H]aspartate during ED was delayed compared to glutamate supporting an initial phase of synaptic glutamate release. Uptake of L-[3H]glutamate was increased during the period of glutamate release, suggesting passive diffusion across the cell membrane or enhanced transport efficacy in cellular elements with functioning uptake mechanisms.

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Section: Discussionsupporting

confidence: 81%

Section: Amino-acid Release Induced By Depolarizationmentioning

confidence: 93%

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Amino-acid release from human cerebral cortex during simulated ischaemia in vitro

Hegstad

Berg-Johnsen

et al. 1996

Acta neurochir

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“…Neurol. 396:51-63, 1998 Indexing terms: synapses; neurons; astrocytes; epilepsy Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the human cerebral cortex (McCormick, 1989;McCormick et al, 1993;Haugstad et al, 1992;Hornung and De Tribolet, 1995). Over the last two decades, research fostered by the development of immunologic and molecular probes has prompted numerous investigations on the organization of the GABAergic system in the human cortex that have provided detailed knowledge of the number, morphology, synaptic relationships, distribution, and ontogeny of cortical GABAergic neurons (Sch-…”

mentioning

confidence: 99%

Neuronal and glial localization of GAT-1, a high-affinity ?-aminobutyric acid plasma membrane transporter, in human cerebral cortex: With a note on its distribution in monkey cortex

et al. 1998

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High-affinity gamma-aminobutyric (GABA) plasma membrane transporters (GATs) influence the action of GABA, the main inhibitory neurotransmitter in the human cerebral cortex. In this study, the cellular expression of GAT-1, the main cortical GABA transporter, was investigated in the human cerebral cortex by using immunocytochemistry with affinity-purified polyclonal antibodies directed to the C-terminus of rat GAT-1. In temporal and prefrontal association cortex (Brodmann's areas 21 and 46) and in cingulofrontal transition cortex (area 32), specific GAT-1 immunoreactivity (ir) was localized to numerous puncta and fibers in all cortical layers. GAT-1+ puncta were distributed homogeneously in all cortical layers, although they were slightly more numerous in layers II-IV, and appeared to have a preferential relationship to the somata and proximal dendrites of unlabeled pyramidal cells, even though, in many cases, they were also observed around nonpyramidal cells. Electron microscopic observations showed that GAT-1+ puncta were axon terminals that formed exclusively symmetric synapses. In addition, some distal astrocytic processes also contained immunoreaction product. Analysis of the patterns of GAT-1 labeling in temporal and prefrontal association areas (21 and 46), in cingulofrontal transition areas (32), and in somatic sensory and motor areas (1 and 4) of the monkey cortex revealed that its distribution varies according to the type of cortex examined and indicated that the distribution of GAT-1 is similar in anatomically corresponding areas of different species. The present study demonstrates that, in the human homotypical cortex, GAT-1 is expressed by both inhibitory axon terminals and astrocytic processes. This localization of GAT-1 is compatible with a major role for this transporter in GABA uptake at GABAergic synapses and suggests that GAT-1 may contribute to determining GABA levels in the extracellular space.

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“…Gamma-amino butyric acid (GABA) is the major inhibitory neurotransmitter in the human cortex (McCormick, 1989;McCormick et al, 1993;Haugstad et al, 1992;Hornung and De Tribolet, 1995), where it plays an important role in physiological and in several pathophysiological conditions, including epilepsy (Meldrum, 1989;Treiman, 2001), schizophrenia (Lewis et al, 1999;Benes and Berretta, 2001), and brain ischemia (Schwartz-Bloom and Sah, 2001).…”

Section: Introductionmentioning

confidence: 99%

Neuronal localization of the GABA transporter GAT-3 in human cerebral cortex: A procedural artifact?

Melone

Barbaresi

Fattorini

et al. 2005

Journal of Chemical Neuroanatomy

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Calcium dependent release of γ-aminobutyric acid (GABA) from human cerebral cortex

Cited by 19 publications

References 22 publications

Amino-acid release from human cerebral cortex during simulated ischaemia in vitro

Amino-acid release from human cerebral cortex during simulated ischaemia in vitro

Neuronal and glial localization of GAT-1, a high-affinity ?-aminobutyric acid plasma membrane transporter, in human cerebral cortex: With a note on its distribution in monkey cortex

Neuronal localization of the GABA transporter GAT-3 in human cerebral cortex: A procedural artifact?

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