Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions
Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hanuska, Adrienn [verfasserIn] Szénási, Gábor [verfasserIn] Albert, Mihaly [verfasserIn] Koles, Laszlo [verfasserIn] Varga, Agoston [verfasserIn] Szabo, Andras [verfasserIn] Matyus, Peter [verfasserIn] Harsing, Laszlo G. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Neurochemical research - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976, 41(2015), 1-2 vom: 12. Sept., Seite 73-85 |
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| Übergeordnetes Werk: |
volume:41 ; year:2015 ; number:1-2 ; day:12 ; month:09 ; pages:73-85 |
| Links: |
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| DOI / URN: |
10.1007/s11064-015-1713-z |
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| Katalog-ID: |
SPR016265181 |
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| 245 | 1 | 0 | |a Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
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| 520 | |a Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. | ||
| 650 | 4 | |a Rat retina |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ischemia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Glycine release |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Glycine transporter |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Glycine transporter inhibitors |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Szénási, Gábor |e verfasserin |4 aut | |
| 700 | 1 | |a Albert, Mihaly |e verfasserin |4 aut | |
| 700 | 1 | |a Koles, Laszlo |e verfasserin |4 aut | |
| 700 | 1 | |a Varga, Agoston |e verfasserin |4 aut | |
| 700 | 1 | |a Szabo, Andras |e verfasserin |4 aut | |
| 700 | 1 | |a Matyus, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Harsing, Laszlo G. |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Neurochemical research |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 |g 41(2015), 1-2 vom: 12. Sept., Seite 73-85 |w (DE-627)320587770 |w (DE-600)2018503-0 |x 1573-6903 |7 nnns |
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10.1007/s11064-015-1713-z doi (DE-627)SPR016265181 (SPR)s11064-015-1713-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Hanuska, Adrienn verfasserin aut Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 Szénási, Gábor verfasserin aut Albert, Mihaly verfasserin aut Koles, Laszlo verfasserin aut Varga, Agoston verfasserin aut Szabo, Andras verfasserin aut Matyus, Peter verfasserin aut Harsing, Laszlo G. verfasserin aut Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 41(2015), 1-2 vom: 12. Sept., Seite 73-85 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 https://dx.doi.org/10.1007/s11064-015-1713-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 41 2015 1-2 12 09 73-85 |
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10.1007/s11064-015-1713-z doi (DE-627)SPR016265181 (SPR)s11064-015-1713-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Hanuska, Adrienn verfasserin aut Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 Szénási, Gábor verfasserin aut Albert, Mihaly verfasserin aut Koles, Laszlo verfasserin aut Varga, Agoston verfasserin aut Szabo, Andras verfasserin aut Matyus, Peter verfasserin aut Harsing, Laszlo G. verfasserin aut Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 41(2015), 1-2 vom: 12. Sept., Seite 73-85 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 https://dx.doi.org/10.1007/s11064-015-1713-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 41 2015 1-2 12 09 73-85 |
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10.1007/s11064-015-1713-z doi (DE-627)SPR016265181 (SPR)s11064-015-1713-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Hanuska, Adrienn verfasserin aut Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 Szénási, Gábor verfasserin aut Albert, Mihaly verfasserin aut Koles, Laszlo verfasserin aut Varga, Agoston verfasserin aut Szabo, Andras verfasserin aut Matyus, Peter verfasserin aut Harsing, Laszlo G. verfasserin aut Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 41(2015), 1-2 vom: 12. Sept., Seite 73-85 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 https://dx.doi.org/10.1007/s11064-015-1713-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 41 2015 1-2 12 09 73-85 |
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10.1007/s11064-015-1713-z doi (DE-627)SPR016265181 (SPR)s11064-015-1713-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Hanuska, Adrienn verfasserin aut Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 Szénási, Gábor verfasserin aut Albert, Mihaly verfasserin aut Koles, Laszlo verfasserin aut Varga, Agoston verfasserin aut Szabo, Andras verfasserin aut Matyus, Peter verfasserin aut Harsing, Laszlo G. verfasserin aut Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 41(2015), 1-2 vom: 12. Sept., Seite 73-85 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 https://dx.doi.org/10.1007/s11064-015-1713-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 41 2015 1-2 12 09 73-85 |
| allfieldsSound |
10.1007/s11064-015-1713-z doi (DE-627)SPR016265181 (SPR)s11064-015-1713-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Hanuska, Adrienn verfasserin aut Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 Szénási, Gábor verfasserin aut Albert, Mihaly verfasserin aut Koles, Laszlo verfasserin aut Varga, Agoston verfasserin aut Szabo, Andras verfasserin aut Matyus, Peter verfasserin aut Harsing, Laszlo G. verfasserin aut Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 41(2015), 1-2 vom: 12. Sept., Seite 73-85 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 https://dx.doi.org/10.1007/s11064-015-1713-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 41 2015 1-2 12 09 73-85 |
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Enthalten in Neurochemical research 41(2015), 1-2 vom: 12. Sept., Seite 73-85 volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 |
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Enthalten in Neurochemical research 41(2015), 1-2 vom: 12. Sept., Seite 73-85 volume:41 year:2015 number:1-2 day:12 month:09 pages:73-85 |
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Rat retina Ischemia Glycine release Glycine transporter Glycine transporter inhibitors |
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Neurochemical research |
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Hanuska, Adrienn @@aut@@ Szénási, Gábor @@aut@@ Albert, Mihaly @@aut@@ Koles, Laszlo @@aut@@ Varga, Agoston @@aut@@ Szabo, Andras @@aut@@ Matyus, Peter @@aut@@ Harsing, Laszlo G. @@aut@@ |
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Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. 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Hanuska, Adrienn |
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Hanuska, Adrienn ddc 610 bkl 44.90 misc Rat retina misc Ischemia misc Glycine release misc Glycine transporter misc Glycine transporter inhibitors Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
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610 ASE 44.90 bkl Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions Rat retina (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Glycine release (dpeaa)DE-He213 Glycine transporter (dpeaa)DE-He213 Glycine transporter inhibitors (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Rat retina misc Ischemia misc Glycine release misc Glycine transporter misc Glycine transporter inhibitors |
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ddc 610 bkl 44.90 misc Rat retina misc Ischemia misc Glycine release misc Glycine transporter misc Glycine transporter inhibitors |
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Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
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| title_full |
Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
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Hanuska, Adrienn |
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Neurochemical research |
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Neurochemical research |
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eng |
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600 - Technology |
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Hanuska, Adrienn Szénási, Gábor Albert, Mihaly Koles, Laszlo Varga, Agoston Szabo, Andras Matyus, Peter Harsing, Laszlo G. |
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Elektronische Aufsätze |
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Hanuska, Adrienn |
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10.1007/s11064-015-1713-z |
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610 |
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verfasserin |
| title_sort |
some operational characteristics of glycine release in rat retina: the role of reverse mode operation of glycine transporter type-1 (glyt-1) in ischemic conditions |
| title_auth |
Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
| abstract |
Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. |
| abstractGer |
Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. |
| abstract_unstemmed |
Abstract Rat posterior eyecups containing the retina were prepared, loaded with [3H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [3H]glycine release, an effect that was found to be external $ Ca^{2+} $-independent. Whereas oxygen and glucose deprivation increased [3H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [3H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [3H]glycine release. Oxygen and glucose deprivation also evoked [3H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [3H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [3H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external $ Ca^{2+} $-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the $ Na^{+} $–$ K^{+} $-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-d-glucose, led to increase of retinal [3H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-d-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [3H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina. |
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Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions |
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Szénási, Gábor Albert, Mihaly Koles, Laszlo Varga, Agoston Szabo, Andras Matyus, Peter Harsing, Laszlo G. |
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| score |
7.400199 |