Biochemical Characteristics of the γ-Aminobutyric Acid System in the Insulinoma Cell Lines HIT-T15, RIN-m5F, βTC3, and Comparison with Rat Brain

Salazar, Pedro; Sánchez-Soto, Marı́a del Carmen; Hiriart, Marcia; Tapia, Ricardo

doi:10.1016/s0188-4409(01)00312-5

Cited by 4 publications

(2 citation statements)

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“…It is reported that insulinoma pancreatic cells possess GAD activity, synthesize GABA and present low GABA uptake [94]. However, different from that reported for brain, pancreatic GAD activity was not enhanced by addition of pyridoxal-5 0 -phosphate.…”

Section: Gaba Uptakecontrasting

confidence: 56%

GABA Effects During Neuronal Differentiation of Stem Cells

2008

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Gamma-amino butyrate (GABA) is the most prevalent inhibitory neurotransmitter in the adult brain. In this review, we summarize the pharmacology and regulation of GABAergic transmission components (biosynthetic enzymes, receptors and transporters) in adult non-neurogenic brain regions. The effects of targeted mutations in genes relevant for GABAergic functions and how they influence specific neuronal circuits and pathological states are presented. We then review GABA actions on neuronal differentiation. During brain development, GABA has depolarizing activity in cerebrocortical neural precursors, controlling cell division and contributing to neuronal migration and maturation. In the adult forebrain there are two neurogenic regions exposed to synaptic and non-synaptic GABA release. Neural stem cells and neuronal progenitors express GABA receptors in subventricular and subgranular zones. GABA effects in these cells are very similar to those found in embryonic cortical precursor cells, and therefore it is possible that this amino acid has important roles during adult brain plasticity.

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Section: Gaba Uptakecontrasting

confidence: 56%

GABA Effects During Neuronal Differentiation of Stem Cells

2008

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“…Whereas cell lines can also be manipulated to over-express GAD65 Thompson et al 2000), little has been reported regarding inherent GAD65 expression or putative GABAergic function for immortalized cell lines during neuronal differentiation. Promoter studies have been performed in the P19 embryonic carcinoma line (Pinal et al 1997), and GAD65 expression has been reported in human fibroblasts and in neuroectodermal and insulinoma cell lines (Kono et al 2001;Salazar et al 2001;Varju et al 2002). The neuronal cell line NTera-2N is negative for GAD65 mRNA (Yoshioka et al 1997), and although PC12 cells have been found to modulate GAD65 and GAD67 expression in response to hypoxia, they are not otherwise GABAergic (Kobayashi and Millhorn 2001).…”

Section: Introductionmentioning

confidence: 99%

GABAergic lineage differentiation of AF5 neural progenitor cells in vitro

et al. 2006

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We have previously described an immortal rat central-nervous-system progenitor cell line, AF5, which is able to exit the cell cycle and assume a differentiated state with neuronal properties. The phenotypic specification of differentiated AF5 cells, however, is not known. In the present study, when induced to differentiate by serum starvation in Neurobasal medium, AF5 cells down-regulate glial fibrillary acidic protein and up-regulate expression of beta-III-tubulin, medium-molecular-weight neurofilament protein, and neuronal growth-associated protein 43. Expression of the gamma-aminobutyric acid (GABA) lineage marker, glutamic acid decarboxylase 67 (GAD67), increases during differentiation, suggesting that AF5 cells adopt a GABAergic lineage. Time-course analysis of the GABAergic neuron specification transcription factor, Pitx2, by reverse transcription/polymerase chain reaction, has shown an increase in the Pitx2 transcript 48 h after initiation of differentiation. In differentiated AF5 cells, expression of the Pitx2 target gene products GAD65 and GABA transporter-1 increases. Cellular GABA levels in differentiated AF5 cells increase by about 26-fold, and GABA release into the medium is 150-fold higher compared with that of undifferentiated cells. Therefore, AF5 cells can be induced to differentiate to a neuronal phenotype with a GABAergic lineage.

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