Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation
Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Adams, Julian [verfasserIn] Collaço-Moraes, Yolanda [verfasserIn] De Belleroche, Jacqueline [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 1996 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 66(1996), 1, Seite 0 |
| Übergeordnetes Werk: |
volume:66 ; year:1996 ; number:1 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1046/j.1471-4159.1996.66010006.x |
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NLEJ24023071X |
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| 520 | |a Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. | ||
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10.1046/j.1471-4159.1996.66010006.x doi (DE-627)NLEJ24023071X DE-627 ger DE-627 rakwb Adams, Julian verfasserin aut Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation Oxford, UK Blackwell Science Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Cyclooxygenase Collaço-Moraes, Yolanda verfasserin aut De Belleroche, Jacqueline verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 66(1996), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:66 year:1996 number:1 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 66 1996 1 0 |
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10.1046/j.1471-4159.1996.66010006.x doi (DE-627)NLEJ24023071X DE-627 ger DE-627 rakwb Adams, Julian verfasserin aut Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation Oxford, UK Blackwell Science Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Cyclooxygenase Collaço-Moraes, Yolanda verfasserin aut De Belleroche, Jacqueline verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 66(1996), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:66 year:1996 number:1 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 66 1996 1 0 |
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10.1046/j.1471-4159.1996.66010006.x doi (DE-627)NLEJ24023071X DE-627 ger DE-627 rakwb Adams, Julian verfasserin aut Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation Oxford, UK Blackwell Science Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Cyclooxygenase Collaço-Moraes, Yolanda verfasserin aut De Belleroche, Jacqueline verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 66(1996), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:66 year:1996 number:1 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 66 1996 1 0 |
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10.1046/j.1471-4159.1996.66010006.x doi (DE-627)NLEJ24023071X DE-627 ger DE-627 rakwb Adams, Julian verfasserin aut Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation Oxford, UK Blackwell Science Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Cyclooxygenase Collaço-Moraes, Yolanda verfasserin aut De Belleroche, Jacqueline verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 66(1996), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:66 year:1996 number:1 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 66 1996 1 0 |
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10.1046/j.1471-4159.1996.66010006.x doi (DE-627)NLEJ24023071X DE-627 ger DE-627 rakwb Adams, Julian verfasserin aut Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation Oxford, UK Blackwell Science Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Cyclooxygenase Collaço-Moraes, Yolanda verfasserin aut De Belleroche, Jacqueline verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 66(1996), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:66 year:1996 number:1 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 66 1996 1 0 |
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Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation |
| author_sort |
Adams, Julian |
| journal |
Journal of neurochemistry |
| journalStr |
Journal of neurochemistry |
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false |
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marc |
| publishDateSort |
1996 |
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zzz |
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| author_browse |
Adams, Julian Collaço-Moraes, Yolanda De Belleroche, Jacqueline |
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66 |
| physical |
Online-Ressource |
| format_se |
Elektronische Aufsätze |
| author-letter |
Adams, Julian |
| doi_str_mv |
10.1046/j.1471-4159.1996.66010006.x |
| author2-role |
verfasserin |
| title_sort |
cyclooxygenase-2 induction in cerebral cortex: an intracellular response to synaptic excitation |
| title_auth |
Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation |
| abstract |
Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. |
| abstractGer |
Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. |
| abstract_unstemmed |
Abstract: We have characterised the induction of the mitogen-inducible form of cyclooxygenase, COX-2, in the rat cerebral cortex in response to excitotoxin injection into the nucleus basalis. This model is associated with intense stimulation of the ascending pathway to the cerebral cortex, seizure activity, and subsequent ipsilateral cortical induction of various immediate early genes (IEGs), including c-fos, c-jun, and zif268, and ornithine decarboxylase enzyme activity and mRNA, all of which processes are sensitive to treatment with the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801. In this study we show that excitotoxin injection also causes a marked induction of COX-2 mRNA in ipsilateral cortex detectable at 1 h and peaking at 4 h, where COX-2 mRNA levels were 19 times those in unoperated animals. Levels of COX-2 mRNA remained significantly elevated at 24 h. The early induction of COX-2 at 1 h was also seen in sham-operated animals, but at 4 h the COX-2 mRNA level was significantly increased (4.4-fold) in animals injected with excitotoxin compared with sham-operated animals. The induction at this time point (4 h) was explored pharmacologically and found to be significantly attenuated by treatment with MK-801 (1.5 mg/kg), lamotrigine (10 mg/kg), which prevents presynaptic glutamate release by blocking voltage-sensitive Na+ channels, and the glucocorticoid dexamethasone (3 mg/kg), which has an indirect inhibitory effect on phospholipase A2 and COX activity. These results demonstrate that the induction of COX-2 mRNA occurs by two distinct mechanisms: the rapid and transient response to tissue damage and a second delayed and more substantial response, which is initiated by excitotoxin stimulation and is mediated by presynaptic glutamate release, NMDA receptor activation, and subsequent phospholipase A2 activity. We propose a model to demonstrate the similarities between COX-2 and IEG mRNA induction and highlight possible mechanistic differences in the nature of the induction by the phospholipase A2 pathway. |
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| title_short |
Cyclooxygenase-2 Induction in Cerebral Cortex: An Intracellular Response to Synaptic Excitation |
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http://dx.doi.org/10.1046/j.1471-4159.1996.66010006.x |
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| author2 |
Collaço-Moraes, Yolanda De Belleroche, Jacqueline |
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