Content and traffic of taurine in hippocampal reactive astrocytes

Junyent, Fèlix; Lemos, Luisa de; Utrera, Juana; Paco, Sonia; Aguado, Fernando; Camins, Antoni; Pallàs, Mercè; Romero, Rafael; Auladell, Carme

doi:10.1002/hipo.20739

Cited by 25 publications

(20 citation statements)

References 64 publications

(76 reference statements)

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“…9). TAU efflux probably occurs mainly from glia (Junyent et al, 2011). However, the mechanism of the observed transient TAU ECF elevation during MeAIB clearance is beyond the scope of the present paper, because the nature of the volume-activated taurine efflux pathway is still controversial (Shennan, 2008).…”

Section: Discussionmentioning

confidence: 99%

Electrographic seizures are significantly reduced by in vivo inhibition of neuronal uptake of extracellular glutamine in rat hippocampus

Kanamori

Ross

2013

Epilepsy Research

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Summary Rats were given unilateral kainate injection into hippocampal CA3 region, and the effect of chronic electrographic seizures on extracellular glutamine (GLNECF) was examined in those with low and steady levels of extracellular glutamate (GLUECF). GLNECF, collected by microdialysis in awake rats for 5 h, decreased to 62 ± 4.4% of the initial concentration (n = 6). This change correlated with the frequency and magnitude of seizure activity, and occurred in the ipsilateral but not in contralateral hippocampus, nor in kainate-injected rats that did not undergo seizure (n = 6). Hippocampal intracellular GLN did not differ between the Seizure and No-Seizure Groups. These results suggested an intriguing possibility that seizure-induced decrease of GLNECF reflects not decreased GLN efflux into the extracellular fluid, but increased uptake into neurons. To examine this possibility, neuronal uptake of GLNECF was inhibited in vivo by intrahippocampal perfusion of 2-(methylamino)isobutyrate, a competitive and reversible inhibitor of the sodium-coupled neutral amino acid transporter (SNAT) subtypes 1 and 2, as demonstrated by 1.8 ± 0.17 fold elevation of GLNECF (n = 7). The frequency of electrographic seizures during uptake inhibition was reduced to 35 ± 7% (n = 7) of the frequency in pre-perfusion period, and returned to 88 ± 9% in the post-perfusion period. These novel in vivo results strongly suggest that, in this well-established animal model of temporal-lobe epilepsy, the observed seizure-induced decrease of GLNECF reflects its increased uptake into neurons to sustain enhanced glutamatergic epileptiform activity, thereby demonstrating a possible new target for anti-seizure therapies.

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Section: Discussionmentioning

confidence: 99%

Electrographic seizures are significantly reduced by in vivo inhibition of neuronal uptake of extracellular glutamine in rat hippocampus

Kanamori

Ross

2013

Epilepsy Research

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“…RNA (1 μg) was used for reverse transcription using high-capacity cDNA of the reverse transcription kit RT (TaKaRa Biotechnology CO., Ltd) according to the manufacturer’s instructions. The PCNA, Cyclin D3, Slc38a1/SNAT1, Slc38a2/SNAT2, Slc38a4/SNAT4, TAUT, Slc2a1/GLUT1, Slc2a3/GLUT3 and GAPDH mRNA primer sequences were designed according to earlier publications155051. RT-qPCR was performed using a Light Cycler Fast Start DNA Master SYBR Green I Kit and an ABI Prism 7300 Sequence Detection System (Applied Biosystems, Foster City, California, USA), and relative gene expression was determined using the 2-ΔΔct method with normalization to GAPDH expression.…”

Section: Methodsmentioning

confidence: 99%

Exposure of pregnant mice to triclosan impairs placental development and nutrient transport

Cao

Wang

et al. 2017

Sci Rep

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Triclosan (TCS) is associated with spontaneous abortions and fetal growth restriction. Here, we showed that when pregnant mice were treated with 8 mg/kg TCS (8-TCS mice) on gestational days (GD) 6–18 fetal body weights were lower than controls. Placental weights and volumes were reduced in 8-TCS mice. The placental proliferative cells and expression of PCNA and Cyclin D3 on GD13 were remarkably decreased in 8-TCS mice. The decreases in activities and expression of placental System A amino acid or glucose transporters on GD14 and GD17 were observed in 8-TCS mice. Levels of serum thyroxine (T4) and triiodothyronine (T3) were lower in 8-TCS mice than those in controls. Declines of placental Akt, mTOR and P70S6K phosphorylation in 8-TCS mice were corrected by L-thyroxinein (T4). Treating 8-TCS mice with T4 rescued the placental cell proliferation and recovered the activity and expression of amino acid and glucose transporters, which were sensitive to mTOR inhibition by rapamycin. Furthermore, the replacement of T4 could rescue the decrease in fetal body weight, which was blocked by rapamycin. These findings indicate that TCS-induced hypothyroxinemia in gestation mice through reducing Akt-mTOR signaling may impair placental development and nutrient transfer leading to decreases in fetal body weight.

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“…A recent report indicates that the taurine level in astrocytes and their TAUT expression can also depend upon their activation state. Taurine level and TAUT expression in astrocytes were increased in the hippocampus during gliosis in mice treated with kainic acid, a murine model of epilepsy [159].…”

Section: Glycinementioning

confidence: 99%

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

et al. 2011

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It is a common and widely accepted assumption that glycine and GABA are the main inhibitory transmitters in the central nervous system (CNS). But, in the past 20 years, several studies have clearly demonstrated that these amino acids can also be excitatory in the immature central nervous system. In addition, it is now established that both GABA receptors (GABARs) and glycine receptors (GlyRs) can be located extrasynaptically and can be activated by paracrine release of endogenous agonists, such as GABA, glycine, and taurine. Recently, non-synaptic release of GABA, glycine, and taurine gained further attention with increasing evidence suggesting a developmental role of these neurotransmitters in neuronal network formation before and during synaptogenesis. This review summarizes recent knowledge about the non-synaptic activation of GABA(A)Rs and GlyRs, both in developing and adult CNS. We first present studies that reveal the functional specialization of both non-synaptic GABA(A)Rs and GlyRs and we discuss the neuronal versus non-neuronal origin of the paracrine release of GABA(A)R and GlyR agonists. We then discuss the proposed non-synaptic release mechanisms and/or pathways for GABA, glycine, and taurine. Finally, we summarize recent data about the various roles of non-synaptic GABAergic and glycinergic systems during the development of neuronal networks and in the adult.

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Content and traffic of taurine in hippocampal reactive astrocytes

Cited by 25 publications

References 64 publications

Electrographic seizures are significantly reduced by in vivo inhibition of neuronal uptake of extracellular glutamine in rat hippocampus

Electrographic seizures are significantly reduced by in vivo inhibition of neuronal uptake of extracellular glutamine in rat hippocampus

Exposure of pregnant mice to triclosan impairs placental development and nutrient transport

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

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