Development of GABAergic neurons and their transporter in human temporal cortex

Hachiya, Yuriko; Takashima, Sachio

doi:10.1016/s0887-8994(01)00348-4

Cited by 14 publications

(13 citation statements)

References 38 publications

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“…On those occasions when paraffin sections have been employed (e.g. Hachiya and Takashima 2001), the results have been in overall accord with earlier studies. A common practice, when using paraffin sections, is to employ antigen recovery.…”

Section: Introductionsupporting

confidence: 88%

“…However, only a limited number of studies has been performed to determine the distribution of GAT-1 in brains of non-rodent species, such as cats (Barbaresi et al 2001), monkeys (Ng and Ong 1999;Erickson and Lewis 2002) and humans (Ong et al 1998;Conti et al 1998;Hachiya and Takashima 2001). These studies have often focused on small brain regions, such as the periaqueductal grey (Barbaresi et al 2001), precluding wider anatomical comparisons between species and have usually employed antibodies against the carboxyl terminal region of the rat sequence of GAT-1.…”

Section: Introductionmentioning

confidence: 99%

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Differential expression of the GABA transporters GAT-1 and GAT-3 in brains of rats, cats, monkeys and humans

et al. 2005

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The homeostasis of GABA is critical to normal brain function. Extracellular levels of GABA are regulated mainly by plasmalemmal gamma-aminobutyric acid (GABA) transporters. Whereas the expression of GABA transporters has been extensively studied in rodents, validation of this data in other species, including humans, has been limited. As this information is crucial for our understanding of therapeutic options in human diseases such as epilepsy, we have compared, by immunocytochemistry, the distributions of the GABA transporters GAT-1 and GAT-3 in rats, cats, monkeys and humans. We demonstrate subtle differences between the results reported in the literature and our results, such as the predominance of GAT-1 labelling in neurons rather than astrocytes in the rat cortex. We note that the optimal localisation of GAT-1 in cats, monkeys and humans requires the use of an antibody against the human sequence carboxyl terminal region of GAT-1 rather than against the slightly different rat sequence. We demonstrate that GAT-3 is localised mainly to astrocytes in hindbrain and midbrain regions of rat brains. However, in species such as cats, monkeys and humans, additional strong immunolabelling of oligodendrocytes has also been observed. We suggest that differences in GAT distribution, especially the expression of GAT-3 by oligodendrocytes in humans, must be accommodated in extrapolating rodent models of GABA homeostasis to humans.

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Section: Introductionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Differential expression of the GABA transporters GAT-1 and GAT-3 in brains of rats, cats, monkeys and humans

et al. 2005

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“…Tiagabine enhanced GABA-ergic currents within hippocampal CA-1 cells from a rat epilepsy model and, thereby, counterbalances neuronal hyperexcitability (Stief et al 2005). A similar stimulation of GABA-ergic neurotransmission might occur within the human temporal cortex and the cerebellum, both areas that display a high density of GAT-1 transporters (Hachiya and Takashima 2001;Swan et al 1994;Takayama and Inoue 2005) finally leading to a neuronal hypometabolism, as it has been observed for pure GABA-A receptor agonists such as lorazepam among normal healthy volunteers (Schreckenberger et al 2004b).…”

Section: Discussionmentioning

confidence: 87%

“…In contrast, no brain area was activated by systemic administration of tiagabine alone. Deep layers of the human right temporal cortex that belong to the entorhinal cortex show a dense expression of GAT-1 transporters and, thereby, are able to modulate hippocampal neuronal activity via GABA-ergic mechanisms (Hachiya and Takashima 2001). Tiagabine enhanced GABA-ergic currents within hippocampal CA-1 cells from a rat epilepsy model and, thereby, counterbalances neuronal hyperexcitability (Stief et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Tiagabine does not attenuate alcohol-induced activation of the human reward system

Fehr¹,

Hohmann²,

Gründer

et al. 2007

Psychopharmacology

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Our ethanol challenge imaging study does not provide supporting evidence that the GAT1 inhibitor tiagabine diminishes the rewarding effects of ethanol. Further PET imaging studies using established anticraving compounds, such as the mu-opioid receptor antagonist naltrexone and antiepileptic drugs affecting the GABA-ergic system more broadly, will provide additional important insights on the interaction between the GABA-ergic and the brain reward system in vivo and the suitability of GABA-ergic drugs as anticraving compounds.

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“…Immunocytochemical and in situ hybridization studies have shown that GAT expression begins during embryonic life and is intense at the perinatal stage (Evans et al 1996;Nelson 1996, 1999;Yan et al 1997;Yan and Ribak 1998;Frahm and Draguhn 2001;Hachiya and Takashima 2001), before the onset of synaptogenesis. At that time, GABA acts as an excitatory neurotransmitter and exerts a trophic action that influences synaptogenesis and neuronal differentiation and survival (Madtes and Redburn 1983;Cherubini et al 1991;Lo Turco et al 1995;review in Varju et al 2001); thus the combined action of the neurotransmitter and of its transporters appears pivotal for the maturation of the nervous tissue.…”

Section: Introductionmentioning

confidence: 99%

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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Development of GABAergic neurons and their transporter in human temporal cortex

Cited by 14 publications

References 38 publications

Differential expression of the GABA transporters GAT-1 and GAT-3 in brains of rats, cats, monkeys and humans

Differential expression of the GABA transporters GAT-1 and GAT-3 in brains of rats, cats, monkeys and humans

Tiagabine does not attenuate alcohol-induced activation of the human reward system

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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