Immunocytochemical localization of seleno-glutathione peroxidase in the adult mouse brain

Trépanier, G.; Furling, Denis; Puymirat, Jack; Mirault, Marc-Édouard

doi:10.1016/0306-4522(96)00222-9

Cited by 71 publications

(54 citation statements)

References 40 publications

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“…Moreover, DCF imaging demonstrated a faster rate of H 2 O 2 amplification in DA neurons with ATZ versus MCS. The enhanced effects of ATZ are consistent with the dominant role of catalase in managing neuronal H 2 O 2 in the SNc: not only is catalase activity 20-fold higher than GSH peroxidase activity (Hung and Lee, 1998), GSH peroxidase is primarily glial, with weak expression in DA neurons (Damier et al, 1993;Trépanier et al, 1996). Whether regulation of K ATP channels by elevated H 2 O 2 is direct or indirect in DA neurons remains to be elucidated.…”

Section: Functional Consequences Of Endogenous H 2 O 2 Elevationmentioning

confidence: 56%

Endogenous Hydrogen Peroxide Regulates the Excitability of Midbrain Dopamine Neurons via ATP-Sensitive Potassium Channels

Avshalumov¹,

Chen²,

Koós³

et al. 2005

J. Neurosci.

146

212

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ATP-sensitive K+(KATP) channels link metabolic state to cell excitability. Here, we examined regulation of KATPchannels in substantia nigra dopamine neurons by hydrogen peroxide (H2O2), which is produced in all cells during aerobic metabolism. Blockade of KATPchannels by glibenclamide (100 nm) or depletion of intracellular H2O2by including catalase, a peroxidase enzyme, in the patch pipette increased the spontaneous firing rate of all dopamine neurons tested in guinea pig midbrain slices. Using fluorescence imaging with dichlorofluorescein to visualize intracellular H2O2, we found that moderate increases in H2O2during partial inhibition of glutathione (GSH) peroxidase by mercaptosuccinate (0.1-0.3 mm) had no effect on dopamine neuron firing rate. However, with greater GSH inhibition (1 mmmercaptosuccinate) or application of exogenous H2O2, 50% of recorded cells showed KATPchannel-dependent hyperpolarization. Responsive cells also hyperpolarized with diazoxide, a selective opener for KATPchannels containing sulfonylurea receptor SUR1 subunits, but not with cromakalim, a selective opener for SUR2-based channels, indicating that SUR1-based KATPchannels conveyed enhanced sensitivity to elevated H2O2. In contrast, when endogenous H2O2levels were increased after inhibition of catalase, the predominant peroxidase in the substantia nigra, with 3-amino-1,2,4-triazole (1 mm), all dopamine neurons responded with glibenclamide-reversible hyperpolarization. Fluorescence imaging of H2O2indicated that catalase inhibition rapidly amplified intracellular H2O2, whereas inhibition of GSH peroxidase, a predominantly glial enzyme, caused a slower, smaller increase, especially in nonresponsive cells. Thus, endogenous H2O2modulates neuronal activity via KATPchannel opening, thereby enhancing the reciprocal relationship between metabolism and excitability.

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Section: Functional Consequences Of Endogenous H 2 O 2 Elevationmentioning

confidence: 56%

Endogenous Hydrogen Peroxide Regulates the Excitability of Midbrain Dopamine Neurons via ATP-Sensitive Potassium Channels

Avshalumov¹,

Chen²,

Koós³

et al. 2005

J. Neurosci.

146

212

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“…A very similar pattern of enhanced GPx enrichment in the hippocampal pyramidal cell layer was found in a second Tg line, Tg-MT-GPx-13 (data not shown). As demonstrated previously (17), appropriate controls showed no detectable immunostaining with preimmune antibody or when the primary antibody was omitted, and staining was largely suppressed when the antibody was preadsorbed with commercial GPx. Therefore, the localized increase of immunoreactivity observed in the pyramidal cell layer of the Tg hippocampus was specific to the GPx antigen.…”

Section: Hippocampal Expression Of Gpx In Tg-gpx1mentioning

confidence: 74%

“…GPx activity was measured by coupled assay with t-butyl hydroperoxide as substrate, as previously described (18). In brief, hippocampi were homogenized in ice-cold 0.1 M potassium phosphate buffer, pH 7.8, containing 1 mM EDTA, 0.5 g͞ml leupeptin, 0.5 g͞ml pepstatin A, 17 g͞ml phenylmethylsulfonyl fluoride using a Kontes homogenizer (pestle SZ 20). Triton X-100 (2% final concentration) was added to the homogenates for 1 h at 4°C, and the samples were centrifuged to remove insoluble materials.…”

Section: Methodsmentioning

confidence: 99%

“…Immunocytochemical analysis of GPx expression in the mouse hippocampal region was performed as described elsewhere (17) by using an immunoaffinity-purified antibody derived from polyclonal antiserum raised against recombinant human GPx1. GPx activity was measured by coupled assay with t-butyl hydroperoxide as substrate, as previously described (18).…”

Section: Methodsmentioning

confidence: 99%

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Impairment of synaptic transmission by transient hypoxia in hippocampal slices: Improved recovery in glutathione peroxidase transgenic mice

Furling

Ghribi

Lahsaini

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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There is increasing evidence that oxygen free radicals contribute to ischemic brain injury. It is unclear, however, to what extent specific antioxidant enzymes can prevent or reverse the impairment of synaptic function caused by transient hypoxia. In this study, we investigated in transgenic (Tg) mice whether a moderate increase in glutathione peroxidase-1 (GPx1) may improve the capacity of CA1 pyramidal cells to recover synaptic transmission after a short period of hypoxia in vitro. In control hippocampal slices, transient hypoxia (7-9 min) produced irreversible loss of excitatory postsynaptic potentials. Complete recovery of synaptic transmission was observed with homozygous Tg-MT-GPx-6 mice after reoxygenation, and, after repeated episodes of hypoxia, synaptic transmission was still viable in most Tg slices, in contrast to non-Tg slices. Moreover, hypoxic episodes abolished the capacity of hippocampal slices to generate long-term potentiation in area CA1 of control mice, whereas a significant extent of long-term potentiation expression was still preserved in Tg tissues. We also demonstrated that susceptibility to N-methyl-D-aspartate-mediated oxidative injury was reduced in Tg hippocampal slices. In conclusion, our results suggest that a moderate GPx increase can be sufficient to prevent irreversible functional damage produced by transient hypoxia in the hippocampus and to help maintain basic electrophysiological mechanisms involved in memory formation.

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“…Forty micrograms of protein extract was separated on 12% sodium dodecyl sulfate/polyacrylamide gel, transferred onto nitrocellulose membranes and the resulting blot was blocked in PBS containing 3% skim milk for 30 min. Each blot was incubated overnight at 4°C with the antibody against GPX (Mirault et al, 1991;Trépanier et al, 1996;Kim et al, 2003) or GRX (Laboratory Frontier, Seoul, Korea; Son et al, 2000) at a 1:1000 dilution, respectively. After washing in PBS, membranes were incubated with a biotinylated goat anti-rabbit antibody for 1 h followed by incubation in avidinbiotin conjugated with horseradish peroxidase (Vectastatin Kit, Vector) at room temperature.…”

Section: Western Blot Analysismentioning

confidence: 99%

Ascorbate attenuates trimethyltin-induced oxidative burden and neuronal degeneration in the rat hippocampus by maintaining glutathione homeostasis

et al. 2005

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Immunocytochemical localization of seleno-glutathione peroxidase in the adult mouse brain

Cited by 71 publications

References 40 publications

Endogenous Hydrogen Peroxide Regulates the Excitability of Midbrain Dopamine Neurons via ATP-Sensitive Potassium Channels

Endogenous Hydrogen Peroxide Regulates the Excitability of Midbrain Dopamine Neurons via ATP-Sensitive Potassium Channels

Impairment of synaptic transmission by transient hypoxia in hippocampal slices: Improved recovery in glutathione peroxidase transgenic mice

Ascorbate attenuates trimethyltin-induced oxidative burden and neuronal degeneration in the rat hippocampus by maintaining glutathione homeostasis

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