Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo
Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in...
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| Autor*in: |
Lukkarainen, Jouko [verfasserIn] Kauppinen, Risto A. [verfasserIn] Koistinaho, Jari [verfasserIn] |
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E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1995 |
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Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 7(1995), 9, Seite 0 |
| Übergeordnetes Werk: |
volume:7 ; year:1995 ; number:9 ; pages:0 |
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| DOI / URN: |
10.1111/j.1460-9568.1995.tb00704.x |
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| 245 | 1 | 0 | |a Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
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| 520 | |a Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. | ||
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| 700 | 1 | |a Kauppinen, Risto A. |e verfasserin |4 aut | |
| 700 | 1 | |a Koistinaho, Jari |e verfasserin |4 aut | |
| 700 | 1 | |a Halmekytö, Maria |4 oth | |
| 700 | 1 | |a Alhonen, Leena |4 oth | |
| 700 | 1 | |a Jänne, Juhani |4 oth | |
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10.1111/j.1460-9568.1995.tb00704.x doi (DE-627)NLEJ239882989 DE-627 ger DE-627 rakwb Lukkarainen, Jouko verfasserin aut Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| transgenic mice Kauppinen, Risto A. verfasserin aut Koistinaho, Jari verfasserin aut Halmekytö, Maria oth Alhonen, Leena oth Jänne, Juhani oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 7(1995), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:7 year:1995 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1995.tb00704.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 7 1995 9 0 |
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10.1111/j.1460-9568.1995.tb00704.x doi (DE-627)NLEJ239882989 DE-627 ger DE-627 rakwb Lukkarainen, Jouko verfasserin aut Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| transgenic mice Kauppinen, Risto A. verfasserin aut Koistinaho, Jari verfasserin aut Halmekytö, Maria oth Alhonen, Leena oth Jänne, Juhani oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 7(1995), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:7 year:1995 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1995.tb00704.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 7 1995 9 0 |
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10.1111/j.1460-9568.1995.tb00704.x doi (DE-627)NLEJ239882989 DE-627 ger DE-627 rakwb Lukkarainen, Jouko verfasserin aut Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| transgenic mice Kauppinen, Risto A. verfasserin aut Koistinaho, Jari verfasserin aut Halmekytö, Maria oth Alhonen, Leena oth Jänne, Juhani oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 7(1995), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:7 year:1995 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1995.tb00704.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 7 1995 9 0 |
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10.1111/j.1460-9568.1995.tb00704.x doi (DE-627)NLEJ239882989 DE-627 ger DE-627 rakwb Lukkarainen, Jouko verfasserin aut Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| transgenic mice Kauppinen, Risto A. verfasserin aut Koistinaho, Jari verfasserin aut Halmekytö, Maria oth Alhonen, Leena oth Jänne, Juhani oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 7(1995), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:7 year:1995 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1995.tb00704.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 7 1995 9 0 |
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10.1111/j.1460-9568.1995.tb00704.x doi (DE-627)NLEJ239882989 DE-627 ger DE-627 rakwb Lukkarainen, Jouko verfasserin aut Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| transgenic mice Kauppinen, Risto A. verfasserin aut Koistinaho, Jari verfasserin aut Halmekytö, Maria oth Alhonen, Leena oth Jänne, Juhani oth In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 7(1995), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:7 year:1995 number:9 pages:0 http://dx.doi.org/10.1111/j.1460-9568.1995.tb00704.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 7 1995 9 0 |
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We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. 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Lukkarainen, Jouko |
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Lukkarainen, Jouko misc transgenic mice Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
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Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo transgenic mice |
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Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
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Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
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cerebral energy metabolism and immediate early gene induction following severe incomplete ischaemia in transgenic mice overexpressing the human ornithine decarboxylase gene: evidence that putrescine is not neurotoxic in vivo |
| title_auth |
Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
| abstract |
Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. |
| abstractGer |
Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. |
| abstract_unstemmed |
Cerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high-energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9- and 3-fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50-fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c-Fos and zif-268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage. |
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Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo |
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