Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo
The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites o...
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| Autor*in: |
Ciriza, I. [verfasserIn] Azcoitia, I. [verfasserIn] Garcia-Segura, L. M. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2004 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2004 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neuroendocrinology - Oxford [u.a.] : Wiley-Blackwell, 1989, 16(2004), 1, Seite 0 |
| Übergeordnetes Werk: |
volume:16 ; year:2004 ; number:1 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1365-2826.2004.01121.x |
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| 520 | |a The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. | ||
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10.1111/j.1365-2826.2004.01121.x doi (DE-627)NLEJ243102143 DE-627 ger DE-627 rakwb Ciriza, I. verfasserin aut Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| dentate gyrus Azcoitia, I. verfasserin aut Garcia-Segura, L. M. verfasserin aut In Journal of neuroendocrinology Oxford [u.a.] : Wiley-Blackwell, 1989 16(2004), 1, Seite 0 Online-Ressource (DE-627)NLEJ243926375 (DE-600)2007386-0 1365-2826 nnns volume:16 year:2004 number:1 pages:0 http://dx.doi.org/10.1111/j.1365-2826.2004.01121.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 2004 1 0 |
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10.1111/j.1365-2826.2004.01121.x doi (DE-627)NLEJ243102143 DE-627 ger DE-627 rakwb Ciriza, I. verfasserin aut Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| dentate gyrus Azcoitia, I. verfasserin aut Garcia-Segura, L. M. verfasserin aut In Journal of neuroendocrinology Oxford [u.a.] : Wiley-Blackwell, 1989 16(2004), 1, Seite 0 Online-Ressource (DE-627)NLEJ243926375 (DE-600)2007386-0 1365-2826 nnns volume:16 year:2004 number:1 pages:0 http://dx.doi.org/10.1111/j.1365-2826.2004.01121.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 2004 1 0 |
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10.1111/j.1365-2826.2004.01121.x doi (DE-627)NLEJ243102143 DE-627 ger DE-627 rakwb Ciriza, I. verfasserin aut Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| dentate gyrus Azcoitia, I. verfasserin aut Garcia-Segura, L. M. verfasserin aut In Journal of neuroendocrinology Oxford [u.a.] : Wiley-Blackwell, 1989 16(2004), 1, Seite 0 Online-Ressource (DE-627)NLEJ243926375 (DE-600)2007386-0 1365-2826 nnns volume:16 year:2004 number:1 pages:0 http://dx.doi.org/10.1111/j.1365-2826.2004.01121.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 2004 1 0 |
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10.1111/j.1365-2826.2004.01121.x doi (DE-627)NLEJ243102143 DE-627 ger DE-627 rakwb Ciriza, I. verfasserin aut Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| dentate gyrus Azcoitia, I. verfasserin aut Garcia-Segura, L. M. verfasserin aut In Journal of neuroendocrinology Oxford [u.a.] : Wiley-Blackwell, 1989 16(2004), 1, Seite 0 Online-Ressource (DE-627)NLEJ243926375 (DE-600)2007386-0 1365-2826 nnns volume:16 year:2004 number:1 pages:0 http://dx.doi.org/10.1111/j.1365-2826.2004.01121.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 2004 1 0 |
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10.1111/j.1365-2826.2004.01121.x doi (DE-627)NLEJ243102143 DE-627 ger DE-627 rakwb Ciriza, I. verfasserin aut Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| dentate gyrus Azcoitia, I. verfasserin aut Garcia-Segura, L. M. verfasserin aut In Journal of neuroendocrinology Oxford [u.a.] : Wiley-Blackwell, 1989 16(2004), 1, Seite 0 Online-Ressource (DE-627)NLEJ243926375 (DE-600)2007386-0 1365-2826 nnns volume:16 year:2004 number:1 pages:0 http://dx.doi.org/10.1111/j.1365-2826.2004.01121.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 16 2004 1 0 |
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Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo dentate gyrus |
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Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo |
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Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo |
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Ciriza, I. |
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Journal of neuroendocrinology |
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Ciriza, I. Azcoitia, I. Garcia-Segura, L. M. |
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Ciriza, I. |
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10.1111/j.1365-2826.2004.01121.x |
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reduced progesterone metabolites protect rat hippocampal neurones from kainic acid excitotoxicity in vivo |
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Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo |
| abstract |
The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. |
| abstractGer |
The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. |
| abstract_unstemmed |
The ovarian hormone progesterone is neuroprotective in some animal models of neurodegeneration. Progesterone actions in the brain may partly be mediated by the locally produced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The neuroprotective effects of these two metabolites of progesterone were assessed in this study. Ovariectomized Wistar rats were injected with kainic acid, to induce excitotoxic neuronal death in the hippocampus, and with different doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. The number of surviving neurones in the hilus of the dentate gyrus of the hippocampus was assessed with the optical disector method. The administration of kainic acid resulted in a significant decrease in the number of hilar neurones and in the induction of vimentin expression in reactive astrocytes, a sign of neural damage. Low doses of 5α-dihydroprogesterone (0.25 and 0.5 mg/kg body weight, b.w.) prevented the loss of hilar neurones and the appearance of vimentin immunoreactivity in astrocytes. Higher doses (1–2 mg/kg b.w.) were not neuroprotective. By contrast, low doses of 3α,5α-tetrahydroprogesterone (0.25–1 mg/kg b.w.) were unable to protect the hilus from kainic acid while higher doses (2–4 mg/kg b.w.) were protective. The different optimal neuroprotective doses of 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone suggest that these two steroids may protect neurones using different mechanisms. The neuroprotective effects of 3α,5α-tetrahydroprogesterone may be exerted by the inhibition of neuronal activity via the GABAA receptor. This latter possibility is supported by the observation that 3β,5α-tetrahydroprogesterone, an isomer of 3α,5α-tetrahydroprogesterone that does not bind to GABAA receptor, was not neuroprotective. In summary, our findings suggest that progesterone neuroprotective effects may be, at least in part, mediated by its reduced metabolites 5α-dihydroprogesterone and 3α,5α-tetrahydroprogesterone. |
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Reduced Progesterone Metabolites Protect Rat Hippocampal Neurones From Kainic Acid Excitotoxicity In Vivo |
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