Is there a non-synaptic component in the K+-stimulated release of GABA in the developing rat cortex?

Balcar, Vladimír J.; Dammasch, I. E.; Wolff, Joachim R.

doi:10.1016/0165-3806(83)90148-7

Cited by 39 publications

(6 citation statements)

References 17 publications

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“…These results are in agreement with previous studies of the ontogeny of calcium-dependent GABA release from developing rat brain slices (Balcar et al, 1983(Balcar et al, , 1986 which found that K+-stimulated [3H]GABA release is initially calcium independent. An additional release that is Ca2+ dependent appears in the second postnatal week, and shows a developmental increase thereafter.…”

Section: Discussionsupporting

confidence: 93%

Developmental Changes in the Calcium Dependency of γ‐Aminobutyric Acid Release from Isolated Growth Cones: Correlation with Growth Cone Morphology

Taylor

Gordon‐Weeks

1989

Journal of Neurochemistry

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We have investigated the development of Ca2+-dependent gamma-[3H]aminobutyric acid [( 3H]GABA) release in superfused growth cone fractions isolated from rats between the postnatal ages of 1 and 11 days. We have compared this release with the overall morphology of the subcellular fractions, and identified those structures taking up [3H]GABA by electron microscopical autoradiography. In fractions isolated from rats between 1 and 5 days, K+-evoked [3H]GABA release was completely independent of extracellular Ca2+. After 5 days a Ca2+ dependency appeared, which increased with age, such that by 10 days approximately 50% of the K+-evoked release was Ca2+ dependent. Electron microscopical analysis showed that, at all ages, large numbers of GABAergic growth cones were present in the subcellular fractions. Up to postnatal day 5, the growth cones were synaptic vesicle sparse but, after this age, increasing numbers of synaptic vesicle-containing growth cones were seen. These results suggest that during maturation of GABAergic growth cones into synapses there is, initially, a mechanism for release that is independent of extracellular Ca2+ and that the appearance of a Ca2+-dependent [3H]GABA release from growth cones correlates with the appearance of synaptic vesicles.

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Section: Discussionsupporting

confidence: 93%

Developmental Changes in the Calcium Dependency of γ‐Aminobutyric Acid Release from Isolated Growth Cones: Correlation with Growth Cone Morphology

Taylor

Gordon‐Weeks

1989

Journal of Neurochemistry

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“…GCPs possess specific uptake mechanisms for GABA and 5-HT but do not exhibit Ca2+-dependent release of these transmitters under the conditions that induce externalization of WGA sites or trigger transmitter exocytosis in synaptosomes (see Bowyer et al, 1987). This result, at least for GABA, is in agreement with data on developing brain slices (Balcar et al, 1983(Balcar et al, , 1986 and on growth cones isolated at different postnatal ages (Lockerbie et al, 1985;Taylor and Gordon-Weeks, 1989), which show that Ca2+-dependent transmitter release appears in the rat only in the second postnatal week. Furthermore, Hume et al (1983) have reported "weak coupling" between stimulation and secretion in growing cholinergic axons.…”

Section: Regulated Plasmalemmal Expansion Versus Transmitter Releasesupporting

confidence: 91%

Regulated plasmalemmal expansion in nerve growth cones.

Lockerbie

Miller

Pfenninger

1991

The Journal of Cell Biology

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Abstract. To study the mechanisms underlying plasmalemmal expansion in the nerve growth cone, a cellfree assay was developed to quantify membrane addition, using ligand binding and sealed growth cone particles isolated by subcellular fractionation from fetal rat brain. Exposed versus total binding sites of t25I-wheat germ agglutinin were measured in the absence or presence of saponin, respectively, after incubation with various agents. Ca2+-ionophore A23187 in the presence of Ca 2+ increases the number of binding sites (Bm~,) but does not change their affinity (Kv), indicating that new receptors appear on the plasma membrane. Similarly, membrane depolarization by high K + or veratridine significantly induces, in a Ca2+-dependent manner, the externalization of lectin binding sites from an internal pool. Morphometric analysis of isolated growth cones indicates that A23187 and high K + treatment cause a significant reduction in a specific cytoplasmic membrane compartment, thus confirming the lectin labeling results and identifying the plasmalemmal precursor. The isolated growth cones take up 7-aminobutyric acid and serotonin, but show no evidence for Ca2+-dependent transmitter release so that transmitter exocytosis is dissociated from plasmalemmal expansion. The data demonstrate that plasmalemmal expansion in the growth cone is a regulated process and identify an internal pool of precursor membrane.

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“…This perikaryal labeling may be due to an intense somatic synthesis and accumulation of the two transporters that only during late development will be targeted to the membrane of distal astrocytic processes. Functionally, the somatic localization of GATs can be related to the diffusion of large amounts of extrasynaptic GABA occurring in a developing brain that lacks mature synaptic terminals and is endowed with large extracellular spaces (Balcar et al 1983;Taylor and Gordon-Weeks 1989;Taylor et al 1990). When GABAergic terminals achieve adult morphology and distribution, by the end of the third postnatal week in the cerebral cortex (Micheva and Beaulieu 1996) and by P15 in the thalamus (De Biasi et al 1997), astrocytes acquire the mature pattern of distribution of GATs, which become concentrated in the plasma membranes of their distal processes, and also of intermediate filaments.…”

Section: Discussionmentioning

confidence: 98%

Expression of GABA transporters, GAT-1 and GAT-3, in the cerebral cortex and thalamus of the rat during postnatal development

Vitellaro‐Zuccarello¹,

Calvaresi²,

Biasi³

2003

Cell Tissue Res

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The cellular and subcellular localization of two GABA transporters, GAT-1 and GAT-3, was investigated using immunocytochemical methods in the rat cerebral cortex and thalamus during postnatal development. The distribution of the transporters is compared with that of the neuronal marker GABA, and with that of vimentin and of glial fibrillary acidic protein, which identify immature and mature astrocytes, respectively. Our observations show that the two transporters are already expressed at birth in both brain areas with the same cellular localization as in adult rats, as GAT-1 is present in growth cones and terminals only in the cortex, whereas both transporters are expressed in astrocytes in the cortex and thalamus. The distribution of GAT-1 and GAT-3 undergoes postnatal changes reflecting in general the neurogenetic events of the neocortex and thalamus and, more specifically, the maturation of GABAergic innervation. The adult-like pattern of expression is achieved in the third postnatal week in the cortex and in the second postnatal week in the thalamus. The early expression of GAT-1 in GABAergic terminals confirms previous studies showing the existence of neuronal mechanisms of GABA uptake from the embryonic stages. As for the glial localization, the precocious existence of two astrocytic GABA transporters suggests that they operate through different functional mechanisms from birth, whereas their exclusively glial expression in the thalamus indicates that the astroglia plays a major role in the transport, recycling and metabolism of thalamic GABA.

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Is there a non-synaptic component in the K+-stimulated release of GABA in the developing rat cortex?

Cited by 39 publications

References 17 publications

Developmental Changes in the Calcium Dependency of γ‐Aminobutyric Acid Release from Isolated Growth Cones: Correlation with Growth Cone Morphology

Developmental Changes in the Calcium Dependency of γ‐Aminobutyric Acid Release from Isolated Growth Cones: Correlation with Growth Cone Morphology

Regulated plasmalemmal expansion in nerve growth cones.

Expression of GABA transporters, GAT-1 and GAT-3, in the cerebral cortex and thalamus of the rat during postnatal development

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