The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation

Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internaliz...
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Autor*in:	Sahlholm, Kristoffer [verfasserIn] Ielacqua, Giovanna D. Xu, Jinbin Jones, Lynne A. Schlegel, Felix Mach, Robert H. Rudin, Markus Schroeter, Aileen

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Arrestin3 Dopamine Dopamine receptor Dopamine agents Eticlopride

Anmerkung:	© The Author(s) 2017

Übergeordnetes Werk:	Enthalten in: Psychopharmacology - Berlin : Springer, 1959, 234(2017), 13 vom: 05. Apr., Seite 2019-2030
Übergeordnetes Werk:	volume:234 ; year:2017 ; number:13 ; day:05 ; month:04 ; pages:2019-2030

Links:	Volltext

DOI / URN:	10.1007/s00213-017-4609-6

Katalog-ID:	SPR002041103

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100	1		\|a Sahlholm, Kristoffer \|e verfasserin \|4 aut
245	1	4	\|a The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
264		1	\|c 2017
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520			\|a Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R.
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650		4	\|a Dopamine agents \|7 (dpeaa)DE-He213
650		4	\|a Eticlopride \|7 (dpeaa)DE-He213
700	1		\|a Ielacqua, Giovanna D. \|4 aut
700	1		\|a Xu, Jinbin \|4 aut
700	1		\|a Jones, Lynne A. \|4 aut
700	1		\|a Schlegel, Felix \|4 aut
700	1		\|a Mach, Robert H. \|4 aut
700	1		\|a Rudin, Markus \|4 aut
700	1		\|a Schroeter, Aileen \|4 aut
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773	1	8	\|g volume:234 \|g year:2017 \|g number:13 \|g day:05 \|g month:04 \|g pages:2019-2030
856	4	0	\|u https://dx.doi.org/10.1007/s00213-017-4609-6 \|z kostenfrei \|3 Volltext
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matchkey_str	article:14322072:2017----::hrlobtarsi2nhpnfrblrsossooa
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publishDate	2017
allfields	10.1007/s00213-017-4609-6 doi (DE-627)SPR002041103 (SPR)s00213-017-4609-6-e DE-627 ger DE-627 rakwb eng Sahlholm, Kristoffer verfasserin aut The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213 Ielacqua, Giovanna D. aut Xu, Jinbin aut Jones, Lynne A. aut Schlegel, Felix aut Mach, Robert H. aut Rudin, Markus aut Schroeter, Aileen aut Enthalten in Psychopharmacology Berlin : Springer, 1959 234(2017), 13 vom: 05. Apr., Seite 2019-2030 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030 https://dx.doi.org/10.1007/s00213-017-4609-6 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_206 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_2056 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 AR 234 2017 13 05 04 2019-2030
spelling	10.1007/s00213-017-4609-6 doi (DE-627)SPR002041103 (SPR)s00213-017-4609-6-e DE-627 ger DE-627 rakwb eng Sahlholm, Kristoffer verfasserin aut The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213 Ielacqua, Giovanna D. aut Xu, Jinbin aut Jones, Lynne A. aut Schlegel, Felix aut Mach, Robert H. aut Rudin, Markus aut Schroeter, Aileen aut Enthalten in Psychopharmacology Berlin : Springer, 1959 234(2017), 13 vom: 05. Apr., Seite 2019-2030 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030 https://dx.doi.org/10.1007/s00213-017-4609-6 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_206 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_2056 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 AR 234 2017 13 05 04 2019-2030
allfields_unstemmed	10.1007/s00213-017-4609-6 doi (DE-627)SPR002041103 (SPR)s00213-017-4609-6-e DE-627 ger DE-627 rakwb eng Sahlholm, Kristoffer verfasserin aut The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213 Ielacqua, Giovanna D. aut Xu, Jinbin aut Jones, Lynne A. aut Schlegel, Felix aut Mach, Robert H. aut Rudin, Markus aut Schroeter, Aileen aut Enthalten in Psychopharmacology Berlin : Springer, 1959 234(2017), 13 vom: 05. Apr., Seite 2019-2030 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030 https://dx.doi.org/10.1007/s00213-017-4609-6 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_206 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_2056 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 AR 234 2017 13 05 04 2019-2030
allfieldsGer	10.1007/s00213-017-4609-6 doi (DE-627)SPR002041103 (SPR)s00213-017-4609-6-e DE-627 ger DE-627 rakwb eng Sahlholm, Kristoffer verfasserin aut The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213 Ielacqua, Giovanna D. aut Xu, Jinbin aut Jones, Lynne A. aut Schlegel, Felix aut Mach, Robert H. aut Rudin, Markus aut Schroeter, Aileen aut Enthalten in Psychopharmacology Berlin : Springer, 1959 234(2017), 13 vom: 05. Apr., Seite 2019-2030 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030 https://dx.doi.org/10.1007/s00213-017-4609-6 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_206 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_2056 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 AR 234 2017 13 05 04 2019-2030
allfieldsSound	10.1007/s00213-017-4609-6 doi (DE-627)SPR002041103 (SPR)s00213-017-4609-6-e DE-627 ger DE-627 rakwb eng Sahlholm, Kristoffer verfasserin aut The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213 Ielacqua, Giovanna D. aut Xu, Jinbin aut Jones, Lynne A. aut Schlegel, Felix aut Mach, Robert H. aut Rudin, Markus aut Schroeter, Aileen aut Enthalten in Psychopharmacology Berlin : Springer, 1959 234(2017), 13 vom: 05. Apr., Seite 2019-2030 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030 https://dx.doi.org/10.1007/s00213-017-4609-6 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_206 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_2056 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 AR 234 2017 13 05 04 2019-2030
language	English
source	Enthalten in Psychopharmacology 234(2017), 13 vom: 05. Apr., Seite 2019-2030 volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030
sourceStr	Enthalten in Psychopharmacology 234(2017), 13 vom: 05. Apr., Seite 2019-2030 volume:234 year:2017 number:13 day:05 month:04 pages:2019-2030
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Arrestin3 Dopamine Dopamine receptor Dopamine agents Eticlopride
isfreeaccess_bool	true
container_title	Psychopharmacology
authorswithroles_txt_mv	Sahlholm, Kristoffer @@aut@@ Ielacqua, Giovanna D. @@aut@@ Xu, Jinbin @@aut@@ Jones, Lynne A. @@aut@@ Schlegel, Felix @@aut@@ Mach, Robert H. @@aut@@ Rudin, Markus @@aut@@ Schroeter, Aileen @@aut@@
publishDateDaySort_date	2017-04-05T00:00:00Z
hierarchy_top_id	341342254
id	SPR002041103
language_de	englisch
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Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. 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author	Sahlholm, Kristoffer
spellingShingle	Sahlholm, Kristoffer misc Arrestin3 misc Dopamine misc Dopamine receptor misc Dopamine agents misc Eticlopride The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
authorStr	Sahlholm, Kristoffer
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topic_title	The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation Arrestin3 (dpeaa)DE-He213 Dopamine (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 Dopamine agents (dpeaa)DE-He213 Eticlopride (dpeaa)DE-He213
topic	misc Arrestin3 misc Dopamine misc Dopamine receptor misc Dopamine agents misc Eticlopride
topic_unstemmed	misc Arrestin3 misc Dopamine misc Dopamine receptor misc Dopamine agents misc Eticlopride
topic_browse	misc Arrestin3 misc Dopamine misc Dopamine receptor misc Dopamine agents misc Eticlopride
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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title	The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
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title_full	The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
author_sort	Sahlholm, Kristoffer
journal	Psychopharmacology
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container_start_page	2019
author_browse	Sahlholm, Kristoffer Ielacqua, Giovanna D. Xu, Jinbin Jones, Lynne A. Schlegel, Felix Mach, Robert H. Rudin, Markus Schroeter, Aileen
container_volume	234
format_se	Elektronische Aufsätze
author-letter	Sahlholm, Kristoffer
doi_str_mv	10.1007/s00213-017-4609-6
title_sort	role of beta-arrestin2 in shaping fmri bold responses to dopaminergic stimulation
title_auth	The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
abstract	Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. © The Author(s) 2017
abstractGer	Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. © The Author(s) 2017
abstract_unstemmed	Rationale The dopamine $ D_{2} $ receptor ($ D_{2} $R) couples to inhibitory $ G_{i/o} $ proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired $ D_{2} $R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of $ D_{2} $R. © The Author(s) 2017
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container_issue	13
title_short	The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
url	https://dx.doi.org/10.1007/s00213-017-4609-6
remote_bool	true
author2	Ielacqua, Giovanna D. Xu, Jinbin Jones, Lynne A. Schlegel, Felix Mach, Robert H. Rudin, Markus Schroeter, Aileen
author2Str	Ielacqua, Giovanna D. Xu, Jinbin Jones, Lynne A. Schlegel, Felix Mach, Robert H. Rudin, Markus Schroeter, Aileen
ppnlink	341342254
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1007/s00213-017-4609-6
up_date	2024-07-04T01:33:21.716Z
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Beta-arrestin2 binds to the intracellular regions of the agonist-occupied $ D_{2} $R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies $ D_{2} $R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the $ D_{2} $R antagonist, eticlopride. 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