Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis
Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for...
Ausführliche Beschreibung
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| Autor*in: |
Müller, Christian P. [verfasserIn] Kalinichenko, Liubov S. [verfasserIn] Tiesel, Jens [verfasserIn] Witt, Matthias [verfasserIn] Stöckl, Thomas [verfasserIn] Sprenger, Eva [verfasserIn] Fuchser, Jens [verfasserIn] Beckmann, Janine [verfasserIn] Praetner, Marc [verfasserIn] Huber, Sabine E. [verfasserIn] Amato, Davide [verfasserIn] Mühle, Christiane [verfasserIn] Büttner, Christian [verfasserIn] Ekici, Arif B. [verfasserIn] Smaga, Irena [verfasserIn] Pomierny-Chamiolo, Lucyna [verfasserIn] Pomierny, Bartosz [verfasserIn] Filip, Malgorzata [verfasserIn] Eulenburg, Volker [verfasserIn] Gulbins, Erich [verfasserIn] Lourdusamy, Anbarasu [verfasserIn] Reichel, Martin [verfasserIn] Kornhuber, Johannes [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Acta neuropathologica - Berlin : Springer, 1961, 133(2016), 3 vom: 20. Dez., Seite 463-483 |
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| Übergeordnetes Werk: |
volume:133 ; year:2016 ; number:3 ; day:20 ; month:12 ; pages:463-483 |
| Links: |
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| DOI / URN: |
10.1007/s00401-016-1658-6 |
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| Katalog-ID: |
SPR004990994 |
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| 245 | 1 | 0 | |a Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis |
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| 520 | |a Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. | ||
| 650 | 4 | |a Alcohol |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Drug instrumentalization |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Depression |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Acid sphingomyelinase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Sphingomyelin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Nucleus accumbens |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Kalinichenko, Liubov S. |e verfasserin |4 aut | |
| 700 | 1 | |a Tiesel, Jens |e verfasserin |4 aut | |
| 700 | 1 | |a Witt, Matthias |e verfasserin |4 aut | |
| 700 | 1 | |a Stöckl, Thomas |e verfasserin |4 aut | |
| 700 | 1 | |a Sprenger, Eva |e verfasserin |4 aut | |
| 700 | 1 | |a Fuchser, Jens |e verfasserin |4 aut | |
| 700 | 1 | |a Beckmann, Janine |e verfasserin |4 aut | |
| 700 | 1 | |a Praetner, Marc |e verfasserin |4 aut | |
| 700 | 1 | |a Huber, Sabine E. |e verfasserin |4 aut | |
| 700 | 1 | |a Amato, Davide |e verfasserin |4 aut | |
| 700 | 1 | |a Mühle, Christiane |e verfasserin |4 aut | |
| 700 | 1 | |a Büttner, Christian |e verfasserin |4 aut | |
| 700 | 1 | |a Ekici, Arif B. |e verfasserin |4 aut | |
| 700 | 1 | |a Smaga, Irena |e verfasserin |4 aut | |
| 700 | 1 | |a Pomierny-Chamiolo, Lucyna |e verfasserin |4 aut | |
| 700 | 1 | |a Pomierny, Bartosz |e verfasserin |4 aut | |
| 700 | 1 | |a Filip, Malgorzata |e verfasserin |4 aut | |
| 700 | 1 | |a Eulenburg, Volker |e verfasserin |4 aut | |
| 700 | 1 | |a Gulbins, Erich |e verfasserin |4 aut | |
| 700 | 1 | |a Lourdusamy, Anbarasu |e verfasserin |4 aut | |
| 700 | 1 | |a Reichel, Martin |e verfasserin |4 aut | |
| 700 | 1 | |a Kornhuber, Johannes |e verfasserin |4 aut | |
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10.1007/s00401-016-1658-6 doi (DE-627)SPR004990994 (SPR)s00401-016-1658-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Müller, Christian P. verfasserin aut Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. Alcohol (dpeaa)DE-He213 Drug instrumentalization (dpeaa)DE-He213 Depression (dpeaa)DE-He213 Acid sphingomyelinase (dpeaa)DE-He213 Sphingomyelin (dpeaa)DE-He213 Nucleus accumbens (dpeaa)DE-He213 Kalinichenko, Liubov S. verfasserin aut Tiesel, Jens verfasserin aut Witt, Matthias verfasserin aut Stöckl, Thomas verfasserin aut Sprenger, Eva verfasserin aut Fuchser, Jens verfasserin aut Beckmann, Janine verfasserin aut Praetner, Marc verfasserin aut Huber, Sabine E. verfasserin aut Amato, Davide verfasserin aut Mühle, Christiane verfasserin aut Büttner, Christian verfasserin aut Ekici, Arif B. verfasserin aut Smaga, Irena verfasserin aut Pomierny-Chamiolo, Lucyna verfasserin aut Pomierny, Bartosz verfasserin aut Filip, Malgorzata verfasserin aut Eulenburg, Volker verfasserin aut Gulbins, Erich verfasserin aut Lourdusamy, Anbarasu verfasserin aut Reichel, Martin verfasserin aut Kornhuber, Johannes verfasserin aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 133(2016), 3 vom: 20. Dez., Seite 463-483 (DE-627)253389666 (DE-600)1458410-4 1432-0533 nnns volume:133 year:2016 number:3 day:20 month:12 pages:463-483 https://dx.doi.org/10.1007/s00401-016-1658-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 133 2016 3 20 12 463-483 |
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10.1007/s00401-016-1658-6 doi (DE-627)SPR004990994 (SPR)s00401-016-1658-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Müller, Christian P. verfasserin aut Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. Alcohol (dpeaa)DE-He213 Drug instrumentalization (dpeaa)DE-He213 Depression (dpeaa)DE-He213 Acid sphingomyelinase (dpeaa)DE-He213 Sphingomyelin (dpeaa)DE-He213 Nucleus accumbens (dpeaa)DE-He213 Kalinichenko, Liubov S. verfasserin aut Tiesel, Jens verfasserin aut Witt, Matthias verfasserin aut Stöckl, Thomas verfasserin aut Sprenger, Eva verfasserin aut Fuchser, Jens verfasserin aut Beckmann, Janine verfasserin aut Praetner, Marc verfasserin aut Huber, Sabine E. verfasserin aut Amato, Davide verfasserin aut Mühle, Christiane verfasserin aut Büttner, Christian verfasserin aut Ekici, Arif B. verfasserin aut Smaga, Irena verfasserin aut Pomierny-Chamiolo, Lucyna verfasserin aut Pomierny, Bartosz verfasserin aut Filip, Malgorzata verfasserin aut Eulenburg, Volker verfasserin aut Gulbins, Erich verfasserin aut Lourdusamy, Anbarasu verfasserin aut Reichel, Martin verfasserin aut Kornhuber, Johannes verfasserin aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 133(2016), 3 vom: 20. Dez., Seite 463-483 (DE-627)253389666 (DE-600)1458410-4 1432-0533 nnns volume:133 year:2016 number:3 day:20 month:12 pages:463-483 https://dx.doi.org/10.1007/s00401-016-1658-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 133 2016 3 20 12 463-483 |
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10.1007/s00401-016-1658-6 doi (DE-627)SPR004990994 (SPR)s00401-016-1658-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Müller, Christian P. verfasserin aut Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. Alcohol (dpeaa)DE-He213 Drug instrumentalization (dpeaa)DE-He213 Depression (dpeaa)DE-He213 Acid sphingomyelinase (dpeaa)DE-He213 Sphingomyelin (dpeaa)DE-He213 Nucleus accumbens (dpeaa)DE-He213 Kalinichenko, Liubov S. verfasserin aut Tiesel, Jens verfasserin aut Witt, Matthias verfasserin aut Stöckl, Thomas verfasserin aut Sprenger, Eva verfasserin aut Fuchser, Jens verfasserin aut Beckmann, Janine verfasserin aut Praetner, Marc verfasserin aut Huber, Sabine E. verfasserin aut Amato, Davide verfasserin aut Mühle, Christiane verfasserin aut Büttner, Christian verfasserin aut Ekici, Arif B. verfasserin aut Smaga, Irena verfasserin aut Pomierny-Chamiolo, Lucyna verfasserin aut Pomierny, Bartosz verfasserin aut Filip, Malgorzata verfasserin aut Eulenburg, Volker verfasserin aut Gulbins, Erich verfasserin aut Lourdusamy, Anbarasu verfasserin aut Reichel, Martin verfasserin aut Kornhuber, Johannes verfasserin aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 133(2016), 3 vom: 20. Dez., Seite 463-483 (DE-627)253389666 (DE-600)1458410-4 1432-0533 nnns volume:133 year:2016 number:3 day:20 month:12 pages:463-483 https://dx.doi.org/10.1007/s00401-016-1658-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 133 2016 3 20 12 463-483 |
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10.1007/s00401-016-1658-6 doi (DE-627)SPR004990994 (SPR)s00401-016-1658-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Müller, Christian P. verfasserin aut Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. Alcohol (dpeaa)DE-He213 Drug instrumentalization (dpeaa)DE-He213 Depression (dpeaa)DE-He213 Acid sphingomyelinase (dpeaa)DE-He213 Sphingomyelin (dpeaa)DE-He213 Nucleus accumbens (dpeaa)DE-He213 Kalinichenko, Liubov S. verfasserin aut Tiesel, Jens verfasserin aut Witt, Matthias verfasserin aut Stöckl, Thomas verfasserin aut Sprenger, Eva verfasserin aut Fuchser, Jens verfasserin aut Beckmann, Janine verfasserin aut Praetner, Marc verfasserin aut Huber, Sabine E. verfasserin aut Amato, Davide verfasserin aut Mühle, Christiane verfasserin aut Büttner, Christian verfasserin aut Ekici, Arif B. verfasserin aut Smaga, Irena verfasserin aut Pomierny-Chamiolo, Lucyna verfasserin aut Pomierny, Bartosz verfasserin aut Filip, Malgorzata verfasserin aut Eulenburg, Volker verfasserin aut Gulbins, Erich verfasserin aut Lourdusamy, Anbarasu verfasserin aut Reichel, Martin verfasserin aut Kornhuber, Johannes verfasserin aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 133(2016), 3 vom: 20. Dez., Seite 463-483 (DE-627)253389666 (DE-600)1458410-4 1432-0533 nnns volume:133 year:2016 number:3 day:20 month:12 pages:463-483 https://dx.doi.org/10.1007/s00401-016-1658-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 133 2016 3 20 12 463-483 |
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10.1007/s00401-016-1658-6 doi (DE-627)SPR004990994 (SPR)s00401-016-1658-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Müller, Christian P. verfasserin aut Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. Alcohol (dpeaa)DE-He213 Drug instrumentalization (dpeaa)DE-He213 Depression (dpeaa)DE-He213 Acid sphingomyelinase (dpeaa)DE-He213 Sphingomyelin (dpeaa)DE-He213 Nucleus accumbens (dpeaa)DE-He213 Kalinichenko, Liubov S. verfasserin aut Tiesel, Jens verfasserin aut Witt, Matthias verfasserin aut Stöckl, Thomas verfasserin aut Sprenger, Eva verfasserin aut Fuchser, Jens verfasserin aut Beckmann, Janine verfasserin aut Praetner, Marc verfasserin aut Huber, Sabine E. verfasserin aut Amato, Davide verfasserin aut Mühle, Christiane verfasserin aut Büttner, Christian verfasserin aut Ekici, Arif B. verfasserin aut Smaga, Irena verfasserin aut Pomierny-Chamiolo, Lucyna verfasserin aut Pomierny, Bartosz verfasserin aut Filip, Malgorzata verfasserin aut Eulenburg, Volker verfasserin aut Gulbins, Erich verfasserin aut Lourdusamy, Anbarasu verfasserin aut Reichel, Martin verfasserin aut Kornhuber, Johannes verfasserin aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 133(2016), 3 vom: 20. Dez., Seite 463-483 (DE-627)253389666 (DE-600)1458410-4 1432-0533 nnns volume:133 year:2016 number:3 day:20 month:12 pages:463-483 https://dx.doi.org/10.1007/s00401-016-1658-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 133 2016 3 20 12 463-483 |
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English |
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Enthalten in Acta neuropathologica 133(2016), 3 vom: 20. Dez., Seite 463-483 volume:133 year:2016 number:3 day:20 month:12 pages:463-483 |
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Enthalten in Acta neuropathologica 133(2016), 3 vom: 20. Dez., Seite 463-483 volume:133 year:2016 number:3 day:20 month:12 pages:463-483 |
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Alcohol Drug instrumentalization Depression Acid sphingomyelinase Sphingomyelin Nucleus accumbens |
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Müller, Christian P. @@aut@@ Kalinichenko, Liubov S. @@aut@@ Tiesel, Jens @@aut@@ Witt, Matthias @@aut@@ Stöckl, Thomas @@aut@@ Sprenger, Eva @@aut@@ Fuchser, Jens @@aut@@ Beckmann, Janine @@aut@@ Praetner, Marc @@aut@@ Huber, Sabine E. @@aut@@ Amato, Davide @@aut@@ Mühle, Christiane @@aut@@ Büttner, Christian @@aut@@ Ekici, Arif B. @@aut@@ Smaga, Irena @@aut@@ Pomierny-Chamiolo, Lucyna @@aut@@ Pomierny, Bartosz @@aut@@ Filip, Malgorzata @@aut@@ Eulenburg, Volker @@aut@@ Gulbins, Erich @@aut@@ Lourdusamy, Anbarasu @@aut@@ Reichel, Martin @@aut@@ Kornhuber, Johannes @@aut@@ |
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2016-12-20T00:00:00Z |
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englisch |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR004990994</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519094450.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201001s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00401-016-1658-6</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR004990994</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00401-016-1658-6-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Müller, Christian P.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. 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Müller, Christian P. ddc 610 bkl 44.90 misc Alcohol misc Drug instrumentalization misc Depression misc Acid sphingomyelinase misc Sphingomyelin misc Nucleus accumbens Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis |
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Müller, Christian P. Kalinichenko, Liubov S. Tiesel, Jens Witt, Matthias Stöckl, Thomas Sprenger, Eva Fuchser, Jens Beckmann, Janine Praetner, Marc Huber, Sabine E. Amato, Davide Mühle, Christiane Büttner, Christian Ekici, Arif B. Smaga, Irena Pomierny-Chamiolo, Lucyna Pomierny, Bartosz Filip, Malgorzata Eulenburg, Volker Gulbins, Erich Lourdusamy, Anbarasu Reichel, Martin Kornhuber, Johannes |
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Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis |
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Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. |
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Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. |
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Abstract Alcohol is a widely consumed drug that can lead to addiction and severe brain damage. However, alcohol is also used as self-medication for psychiatric problems, such as depression, frequently resulting in depression-alcoholism comorbidity. Here, we identify the first molecular mechanism for alcohol use with the goal to self-medicate and ameliorate the behavioral symptoms of a genetically induced innate depression. An induced over-expression of acid sphingomyelinase (ASM), as was observed in depressed patients, enhanced the consumption of alcohol in a mouse model of depression. ASM hyperactivity facilitates the establishment of the conditioned behavioral effects of alcohol, and thus drug memories. Opposite effects on drinking and alcohol reward learning were observed in animals with reduced ASM function. Importantly, free-choice alcohol drinking—but not forced alcohol exposure—reduces depression-like behavior selectively in depressed animals through the normalization of brain ASM activity. No such effects were observed in normal mice. ASM hyperactivity caused sphingolipid and subsequent monoamine transmitter hypo-activity in the brain. Free-choice alcohol drinking restores nucleus accumbens sphingolipid- and monoamine homeostasis selectively in depressed mice. A gene expression analysis suggested strong control of ASM on the expression of genes related to the regulation of pH, ion transmembrane transport, behavioral fear response, neuroprotection and neuropeptide signaling pathways. These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis. Both emerge as a new treatment target specifically for depression-induced alcoholism. |
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