Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats
Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Meier, Eddi [verfasserIn] Jørgensen, Ole Steen [verfasserIn] Schousboe, Arne [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1987 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 49(1987), 5, Seite 0 |
| Übergeordnetes Werk: |
volume:49 ; year:1987 ; number:5 ; pages:0 |
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| DOI / URN: |
10.1111/j.1471-4159.1987.tb01015.x |
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| 520 | |a Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. | ||
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10.1111/j.1471-4159.1987.tb01015.x doi (DE-627)NLEJ24028500X DE-627 ger DE-627 rakwb Meier, Eddi verfasserin aut Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats Oxford, UK Blackwell Publishing Ltd 1987 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Neural development Jørgensen, Ole Steen verfasserin aut Schousboe, Arne verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 49(1987), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:49 year:1987 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1987.tb01015.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 49 1987 5 0 |
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10.1111/j.1471-4159.1987.tb01015.x doi (DE-627)NLEJ24028500X DE-627 ger DE-627 rakwb Meier, Eddi verfasserin aut Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats Oxford, UK Blackwell Publishing Ltd 1987 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Neural development Jørgensen, Ole Steen verfasserin aut Schousboe, Arne verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 49(1987), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:49 year:1987 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1987.tb01015.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 49 1987 5 0 |
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10.1111/j.1471-4159.1987.tb01015.x doi (DE-627)NLEJ24028500X DE-627 ger DE-627 rakwb Meier, Eddi verfasserin aut Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats Oxford, UK Blackwell Publishing Ltd 1987 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Neural development Jørgensen, Ole Steen verfasserin aut Schousboe, Arne verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 49(1987), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:49 year:1987 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1987.tb01015.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 49 1987 5 0 |
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10.1111/j.1471-4159.1987.tb01015.x doi (DE-627)NLEJ24028500X DE-627 ger DE-627 rakwb Meier, Eddi verfasserin aut Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats Oxford, UK Blackwell Publishing Ltd 1987 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Neural development Jørgensen, Ole Steen verfasserin aut Schousboe, Arne verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 49(1987), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:49 year:1987 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1987.tb01015.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 49 1987 5 0 |
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10.1111/j.1471-4159.1987.tb01015.x doi (DE-627)NLEJ24028500X DE-627 ger DE-627 rakwb Meier, Eddi verfasserin aut Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats Oxford, UK Blackwell Publishing Ltd 1987 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Neural development Jørgensen, Ole Steen verfasserin aut Schousboe, Arne verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 49(1987), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:49 year:1987 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1987.tb01015.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 49 1987 5 0 |
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Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. |
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Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. |
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Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ24028500X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707105626.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120426s1987 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1471-4159.1987.tb01015.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ24028500X</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Meier, Eddi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Effect of Repeated Treatment with a γ-Aminobutyric Acid Receptor Agonist on Postnatal Neural Development in Rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Publishing Ltd</subfield><subfield code="c">1987</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract: The effect of treatment with the γ-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1-and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. 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