Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission
Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availab...
Ausführliche Beschreibung
Autor*in: |
Maarten Ooms [verfasserIn] Sofie Celen [verfasserIn] Ronald De Hoogt [verfasserIn] Ilse Lenaerts [verfasserIn] Johnny Liebregts [verfasserIn] Greet Vanhoof [verfasserIn] Xavier Langlois [verfasserIn] Andrey Postnov [verfasserIn] Michel Koole [verfasserIn] Alfons Verbruggen [verfasserIn] Koen Van Laere [verfasserIn] Guy Bormans [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Übergeordnetes Werk: |
In: EJNMMI Radiopharmacy and Chemistry - SpringerOpen, 2018, 1(2016), 1, Seite 17 |
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Übergeordnetes Werk: |
volume:1 ; year:2016 ; number:1 ; pages:17 |
Links: |
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DOI / URN: |
10.1186/s41181-016-0005-5 |
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Katalog-ID: |
DOAJ039725987 |
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520 | |a Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. | ||
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700 | 0 | |a Guy Bormans |e verfasserin |4 aut | |
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10.1186/s41181-016-0005-5 doi (DE-627)DOAJ039725987 (DE-599)DOAJd4dd4237d5784bcaae606d3049b031e4 DE-627 ger DE-627 rakwb eng R895-920 RM1-950 Maarten Ooms verfasserin aut Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology Sofie Celen verfasserin aut Ronald De Hoogt verfasserin aut Ilse Lenaerts verfasserin aut Johnny Liebregts verfasserin aut Greet Vanhoof verfasserin aut Xavier Langlois verfasserin aut Andrey Postnov verfasserin aut Michel Koole verfasserin aut Alfons Verbruggen verfasserin aut Koen Van Laere verfasserin aut Guy Bormans verfasserin aut In EJNMMI Radiopharmacy and Chemistry SpringerOpen, 2018 1(2016), 1, Seite 17 (DE-627)844386367 (DE-600)2843088-8 2365421X nnns volume:1 year:2016 number:1 pages:17 https://doi.org/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 kostenfrei http://link.springer.com/article/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/toc/2365-421X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2016 1 17 |
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10.1186/s41181-016-0005-5 doi (DE-627)DOAJ039725987 (DE-599)DOAJd4dd4237d5784bcaae606d3049b031e4 DE-627 ger DE-627 rakwb eng R895-920 RM1-950 Maarten Ooms verfasserin aut Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology Sofie Celen verfasserin aut Ronald De Hoogt verfasserin aut Ilse Lenaerts verfasserin aut Johnny Liebregts verfasserin aut Greet Vanhoof verfasserin aut Xavier Langlois verfasserin aut Andrey Postnov verfasserin aut Michel Koole verfasserin aut Alfons Verbruggen verfasserin aut Koen Van Laere verfasserin aut Guy Bormans verfasserin aut In EJNMMI Radiopharmacy and Chemistry SpringerOpen, 2018 1(2016), 1, Seite 17 (DE-627)844386367 (DE-600)2843088-8 2365421X nnns volume:1 year:2016 number:1 pages:17 https://doi.org/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 kostenfrei http://link.springer.com/article/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/toc/2365-421X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2016 1 17 |
allfields_unstemmed |
10.1186/s41181-016-0005-5 doi (DE-627)DOAJ039725987 (DE-599)DOAJd4dd4237d5784bcaae606d3049b031e4 DE-627 ger DE-627 rakwb eng R895-920 RM1-950 Maarten Ooms verfasserin aut Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology Sofie Celen verfasserin aut Ronald De Hoogt verfasserin aut Ilse Lenaerts verfasserin aut Johnny Liebregts verfasserin aut Greet Vanhoof verfasserin aut Xavier Langlois verfasserin aut Andrey Postnov verfasserin aut Michel Koole verfasserin aut Alfons Verbruggen verfasserin aut Koen Van Laere verfasserin aut Guy Bormans verfasserin aut In EJNMMI Radiopharmacy and Chemistry SpringerOpen, 2018 1(2016), 1, Seite 17 (DE-627)844386367 (DE-600)2843088-8 2365421X nnns volume:1 year:2016 number:1 pages:17 https://doi.org/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 kostenfrei http://link.springer.com/article/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/toc/2365-421X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2016 1 17 |
allfieldsGer |
10.1186/s41181-016-0005-5 doi (DE-627)DOAJ039725987 (DE-599)DOAJd4dd4237d5784bcaae606d3049b031e4 DE-627 ger DE-627 rakwb eng R895-920 RM1-950 Maarten Ooms verfasserin aut Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology Sofie Celen verfasserin aut Ronald De Hoogt verfasserin aut Ilse Lenaerts verfasserin aut Johnny Liebregts verfasserin aut Greet Vanhoof verfasserin aut Xavier Langlois verfasserin aut Andrey Postnov verfasserin aut Michel Koole verfasserin aut Alfons Verbruggen verfasserin aut Koen Van Laere verfasserin aut Guy Bormans verfasserin aut In EJNMMI Radiopharmacy and Chemistry SpringerOpen, 2018 1(2016), 1, Seite 17 (DE-627)844386367 (DE-600)2843088-8 2365421X nnns volume:1 year:2016 number:1 pages:17 https://doi.org/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 kostenfrei http://link.springer.com/article/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/toc/2365-421X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2016 1 17 |
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10.1186/s41181-016-0005-5 doi (DE-627)DOAJ039725987 (DE-599)DOAJd4dd4237d5784bcaae606d3049b031e4 DE-627 ger DE-627 rakwb eng R895-920 RM1-950 Maarten Ooms verfasserin aut Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology Sofie Celen verfasserin aut Ronald De Hoogt verfasserin aut Ilse Lenaerts verfasserin aut Johnny Liebregts verfasserin aut Greet Vanhoof verfasserin aut Xavier Langlois verfasserin aut Andrey Postnov verfasserin aut Michel Koole verfasserin aut Alfons Verbruggen verfasserin aut Koen Van Laere verfasserin aut Guy Bormans verfasserin aut In EJNMMI Radiopharmacy and Chemistry SpringerOpen, 2018 1(2016), 1, Seite 17 (DE-627)844386367 (DE-600)2843088-8 2365421X nnns volume:1 year:2016 number:1 pages:17 https://doi.org/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 kostenfrei http://link.springer.com/article/10.1186/s41181-016-0005-5 kostenfrei https://doaj.org/toc/2365-421X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2016 1 17 |
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Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission |
abstract |
Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. |
abstractGer |
Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. |
abstract_unstemmed |
Abstract Background Phosphodiesterase 10A (PDE10A) is an important regulator of nigrostriatal dopamine (DA) neurotransmission. However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. Conclusions Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking. This study suggests a potential pharmacological interaction between PDE10A enzymes and drugs modifying DA neurotransmission. Therefore, PDE10A binding in patients with neuropsychiatric disorders might be modulated by chronic DA-related treatment. |
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title_short |
Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission |
url |
https://doi.org/10.1186/s41181-016-0005-5 https://doaj.org/article/d4dd4237d5784bcaae606d3049b031e4 http://link.springer.com/article/10.1186/s41181-016-0005-5 https://doaj.org/toc/2365-421X |
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Sofie Celen Ronald De Hoogt Ilse Lenaerts Johnny Liebregts Greet Vanhoof Xavier Langlois Andrey Postnov Michel Koole Alfons Verbruggen Koen Van Laere Guy Bormans |
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Sofie Celen Ronald De Hoogt Ilse Lenaerts Johnny Liebregts Greet Vanhoof Xavier Langlois Andrey Postnov Michel Koole Alfons Verbruggen Koen Van Laere Guy Bormans |
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up_date |
2024-07-04T00:30:07.058Z |
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However, little is known on the effect of alterations in DA neurotransmission on PDE10A availability. Here, we used [18F]JNJ42259152 PET to measure changes in PDE10A availability, secondary to pharmacological alterations in DA release and to investigate whether these are D1- or D2-receptor driven. Results Acute treatment of rats using D-amphetamine (5 mg, s.c. and 1 mg/kg i.v.) did not result in a significant change in PDE10A BPND compared to baseline conditions. 5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03). Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03). Treatment with only SCH23390 further decreased PDE10A binding (-26 %, p = 0.03). No significant alterations in PDE10A mRNA levels were observed. 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