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...
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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]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging

Übergeordnetes Werk:	In: EJNMMI Radiopharmacy and Chemistry - SpringerOpen, 2018, 1(2016), 1, Seite 17
Übergeordnetes Werk:	volume:1 ; year:2016 ; number:1 ; pages:17

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s41181-016-0005-5

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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allfields	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
spelling	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
allfieldsSound	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
language	English
source	In EJNMMI Radiopharmacy and Chemistry 1(2016), 1, Seite 17 volume:1 year:2016 number:1 pages:17
sourceStr	In EJNMMI Radiopharmacy and Chemistry 1(2016), 1, Seite 17 volume:1 year:2016 number:1 pages:17
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging Medical physics. Medical radiology. Nuclear medicine Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	EJNMMI Radiopharmacy and Chemistry
authorswithroles_txt_mv	Maarten Ooms @@aut@@ Sofie Celen @@aut@@ Ronald De Hoogt @@aut@@ Ilse Lenaerts @@aut@@ Johnny Liebregts @@aut@@ Greet Vanhoof @@aut@@ Xavier Langlois @@aut@@ Andrey Postnov @@aut@@ Michel Koole @@aut@@ Alfons Verbruggen @@aut@@ Koen Van Laere @@aut@@ Guy Bormans @@aut@@
publishDateDaySort_date	2016-01-01T00:00:00Z
hierarchy_top_id	844386367
id	DOAJ039725987
language_de	englisch
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callnumber-first	R - Medicine
author	Maarten Ooms
spellingShingle	Maarten Ooms misc R895-920 misc RM1-950 misc Phosphodiesterase 10A misc Dopamine neurotransmission misc D-amphetamine misc Small animal PET misc Brain imaging misc Medical physics. Medical radiology. Nuclear medicine misc Therapeutics. Pharmacology Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission
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topic_title	R895-920 RM1-950 Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission Phosphodiesterase 10A Dopamine neurotransmission D-amphetamine Small animal PET Brain imaging
topic	misc R895-920 misc RM1-950 misc Phosphodiesterase 10A misc Dopamine neurotransmission misc D-amphetamine misc Small animal PET misc Brain imaging misc Medical physics. Medical radiology. Nuclear medicine misc Therapeutics. Pharmacology
topic_unstemmed	misc R895-920 misc RM1-950 misc Phosphodiesterase 10A misc Dopamine neurotransmission misc D-amphetamine misc Small animal PET misc Brain imaging misc Medical physics. Medical radiology. Nuclear medicine misc Therapeutics. Pharmacology
topic_browse	misc R895-920 misc RM1-950 misc Phosphodiesterase 10A misc Dopamine neurotransmission misc D-amphetamine misc Small animal PET misc Brain imaging misc Medical physics. Medical radiology. Nuclear medicine misc Therapeutics. Pharmacology
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title	Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission
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title_full	Striatal phosphodiesterase 10A availability is altered secondary to chronic changes in dopamine neurotransmission
author_sort	Maarten Ooms
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author_browse	Maarten Ooms 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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title_sort	striatal phosphodiesterase 10a availability is altered secondary to chronic changes in dopamine neurotransmission
callnumber	R895-920
title_auth	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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author2	Sofie Celen Ronald De Hoogt Ilse Lenaerts Johnny Liebregts Greet Vanhoof Xavier Langlois Andrey Postnov Michel Koole Alfons Verbruggen Koen Van Laere Guy Bormans
author2Str	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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