Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus
Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the ex...
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| Autor*in: |
Miyazaki, Hiroyuki [verfasserIn] Ono, Takashi [verfasserIn] Okuma, Yasunobu [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2000 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 12(2000), 6, Seite 0 |
| Übergeordnetes Werk: |
volume:12 ; year:2000 ; number:6 ; pages:0 |
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| DOI / URN: |
10.1046/j.1460-9568.2000.00092.x |
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| 520 | |a Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. | ||
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10.1046/j.1460-9568.2000.00092.x doi (DE-627)NLEJ242439934 DE-627 ger DE-627 rakwb Miyazaki, Hiroyuki verfasserin aut Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| CA1 Ono, Takashi verfasserin aut Okuma, Yasunobu verfasserin aut Nagashima, Kazuo oth Nomura, Yasuyuki oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:6 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.00092.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 6 0 |
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10.1046/j.1460-9568.2000.00092.x doi (DE-627)NLEJ242439934 DE-627 ger DE-627 rakwb Miyazaki, Hiroyuki verfasserin aut Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| CA1 Ono, Takashi verfasserin aut Okuma, Yasunobu verfasserin aut Nagashima, Kazuo oth Nomura, Yasuyuki oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:6 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.00092.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 6 0 |
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10.1046/j.1460-9568.2000.00092.x doi (DE-627)NLEJ242439934 DE-627 ger DE-627 rakwb Miyazaki, Hiroyuki verfasserin aut Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| CA1 Ono, Takashi verfasserin aut Okuma, Yasunobu verfasserin aut Nagashima, Kazuo oth Nomura, Yasuyuki oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:6 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.00092.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 6 0 |
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10.1046/j.1460-9568.2000.00092.x doi (DE-627)NLEJ242439934 DE-627 ger DE-627 rakwb Miyazaki, Hiroyuki verfasserin aut Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| CA1 Ono, Takashi verfasserin aut Okuma, Yasunobu verfasserin aut Nagashima, Kazuo oth Nomura, Yasuyuki oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:6 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.00092.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 6 0 |
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10.1046/j.1460-9568.2000.00092.x doi (DE-627)NLEJ242439934 DE-627 ger DE-627 rakwb Miyazaki, Hiroyuki verfasserin aut Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| CA1 Ono, Takashi verfasserin aut Okuma, Yasunobu verfasserin aut Nagashima, Kazuo oth Nomura, Yasuyuki oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:6 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.00092.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 6 0 |
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Glial cell line-derived neurotrophic factor modulates ischemia-induced tyrosine hydroxylase expression in rat hippocampus |
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Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. |
| abstractGer |
Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. |
| abstract_unstemmed |
Recently, we have reported that glial cell line-derived neurotrophic factor (GDNF), which supports the survival of dopaminergic neurons, prevents delayed neuronal death in the hippocampal CA1 region induced by transient forebrain ischemia. In the present study, we examined the role of GDNF in the expression of tyrosine hydroxylase (TH) mRNA induced by transient forebrain ischemia in rats. The expression of TH mRNA was increased in a time-dependent manner, with a significant increase in 24 h to 7 days, in the hippocampus after induction of transient forebrain ischemia, as determined using the reverse transcription and polymerase chain reaction method. Although it has been suggested that the increase of dopamine β-hydroxylase mRNA expression correlates with the activation of noradrenergic neurons, no increase of dopamine β-hydroxylase mRNA in the hippocampus was observed in our system. Western blot analysis revealed that TH protein, but not dopamine β-hydroxylase protein, was produced in a time-dependent manner in the hippocampus during the ischemia. Interestingly, the induction level of TH mRNA was reduced by intrahippocampal microinjection of GDNF (1.0 μg), and this local GDNF treatment also reduced the increase of TH-like immunohistochemistry-positive terminals in the hippocampus. In contrast, local GDNF treatment of normal rats increased the TH mRNA expression at 6–12 h. These findings suggest that GDNF protects against neuronal degeneration including delayed neuronal death in the hippocampal CA1 region by modulating the expression levels of TH mRNA and protein. |
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