Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface

Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Waddington, John L. [verfasserIn] O'Tuathaigh, Colm O'Sullivan, Gerard Tomiyama, Katsunori Koshikawa, Noriaki Croke, David T.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2005

Schlagwörter:	Dopamine D , D and D receptor subtypes Gα Gγ Adenylyl cyclase PKA DARPP-32 ‘Knockout’ Transgenic Behavioural phenotype Ethogram Orofacial movements

Anmerkung:	© Springer-Verlag 2005

Übergeordnetes Werk:	Enthalten in: Psychopharmacology - Berlin : Springer, 1959, 181(2005), 4 vom: 22. Juli, Seite 611-638
Übergeordnetes Werk:	volume:181 ; year:2005 ; number:4 ; day:22 ; month:07 ; pages:611-638

Links:	Volltext

DOI / URN:	10.1007/s00213-005-0058-8

Katalog-ID:	SPR001996460

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520			\|a Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge.
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publishDate	2005
allfields	10.1007/s00213-005-0058-8 doi (DE-627)SPR001996460 (SPR)s00213-005-0058-8-e DE-627 ger DE-627 rakwb eng Waddington, John L. verfasserin aut Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213 O'Tuathaigh, Colm aut O'Sullivan, Gerard aut Tomiyama, Katsunori aut Koshikawa, Noriaki aut Croke, David T. aut Enthalten in Psychopharmacology Berlin : Springer, 1959 181(2005), 4 vom: 22. Juli, Seite 611-638 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:181 year:2005 number:4 day:22 month:07 pages:611-638 https://dx.doi.org/10.1007/s00213-005-0058-8 lizenzpflichtig 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 181 2005 4 22 07 611-638
spelling	10.1007/s00213-005-0058-8 doi (DE-627)SPR001996460 (SPR)s00213-005-0058-8-e DE-627 ger DE-627 rakwb eng Waddington, John L. verfasserin aut Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213 O'Tuathaigh, Colm aut O'Sullivan, Gerard aut Tomiyama, Katsunori aut Koshikawa, Noriaki aut Croke, David T. aut Enthalten in Psychopharmacology Berlin : Springer, 1959 181(2005), 4 vom: 22. Juli, Seite 611-638 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:181 year:2005 number:4 day:22 month:07 pages:611-638 https://dx.doi.org/10.1007/s00213-005-0058-8 lizenzpflichtig 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 181 2005 4 22 07 611-638
allfields_unstemmed	10.1007/s00213-005-0058-8 doi (DE-627)SPR001996460 (SPR)s00213-005-0058-8-e DE-627 ger DE-627 rakwb eng Waddington, John L. verfasserin aut Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213 O'Tuathaigh, Colm aut O'Sullivan, Gerard aut Tomiyama, Katsunori aut Koshikawa, Noriaki aut Croke, David T. aut Enthalten in Psychopharmacology Berlin : Springer, 1959 181(2005), 4 vom: 22. Juli, Seite 611-638 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:181 year:2005 number:4 day:22 month:07 pages:611-638 https://dx.doi.org/10.1007/s00213-005-0058-8 lizenzpflichtig 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 181 2005 4 22 07 611-638
allfieldsGer	10.1007/s00213-005-0058-8 doi (DE-627)SPR001996460 (SPR)s00213-005-0058-8-e DE-627 ger DE-627 rakwb eng Waddington, John L. verfasserin aut Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213 O'Tuathaigh, Colm aut O'Sullivan, Gerard aut Tomiyama, Katsunori aut Koshikawa, Noriaki aut Croke, David T. aut Enthalten in Psychopharmacology Berlin : Springer, 1959 181(2005), 4 vom: 22. Juli, Seite 611-638 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:181 year:2005 number:4 day:22 month:07 pages:611-638 https://dx.doi.org/10.1007/s00213-005-0058-8 lizenzpflichtig 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 181 2005 4 22 07 611-638
allfieldsSound	10.1007/s00213-005-0058-8 doi (DE-627)SPR001996460 (SPR)s00213-005-0058-8-e DE-627 ger DE-627 rakwb eng Waddington, John L. verfasserin aut Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213 O'Tuathaigh, Colm aut O'Sullivan, Gerard aut Tomiyama, Katsunori aut Koshikawa, Noriaki aut Croke, David T. aut Enthalten in Psychopharmacology Berlin : Springer, 1959 181(2005), 4 vom: 22. Juli, Seite 611-638 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:181 year:2005 number:4 day:22 month:07 pages:611-638 https://dx.doi.org/10.1007/s00213-005-0058-8 lizenzpflichtig 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 181 2005 4 22 07 611-638
language	English
source	Enthalten in Psychopharmacology 181(2005), 4 vom: 22. Juli, Seite 611-638 volume:181 year:2005 number:4 day:22 month:07 pages:611-638
sourceStr	Enthalten in Psychopharmacology 181(2005), 4 vom: 22. Juli, Seite 611-638 volume:181 year:2005 number:4 day:22 month:07 pages:611-638
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Dopamine D , D and D receptor subtypes Gα Gγ Adenylyl cyclase PKA DARPP-32 ‘Knockout’ Transgenic Behavioural phenotype Ethogram Orofacial movements
isfreeaccess_bool	false
container_title	Psychopharmacology
authorswithroles_txt_mv	Waddington, John L. @@aut@@ O'Tuathaigh, Colm @@aut@@ O'Sullivan, Gerard @@aut@@ Tomiyama, Katsunori @@aut@@ Koshikawa, Noriaki @@aut@@ Croke, David T. @@aut@@
publishDateDaySort_date	2005-07-22T00:00:00Z
hierarchy_top_id	341342254
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However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. 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author	Waddington, John L.
spellingShingle	Waddington, John L. misc Dopamine D misc , D misc and D misc receptor subtypes misc Gα misc Gγ misc Adenylyl cyclase misc PKA misc DARPP-32 misc ‘Knockout’ misc Transgenic misc Behavioural phenotype misc Ethogram misc Orofacial movements Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
authorStr	Waddington, John L.
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topic_title	Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface Dopamine D (dpeaa)DE-He213 , D (dpeaa)DE-He213 and D (dpeaa)DE-He213 receptor subtypes (dpeaa)DE-He213 Gα (dpeaa)DE-He213 Gγ (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 PKA (dpeaa)DE-He213 DARPP-32 (dpeaa)DE-He213 ‘Knockout’ (dpeaa)DE-He213 Transgenic (dpeaa)DE-He213 Behavioural phenotype (dpeaa)DE-He213 Ethogram (dpeaa)DE-He213 Orofacial movements (dpeaa)DE-He213
topic	misc Dopamine D misc , D misc and D misc receptor subtypes misc Gα misc Gγ misc Adenylyl cyclase misc PKA misc DARPP-32 misc ‘Knockout’ misc Transgenic misc Behavioural phenotype misc Ethogram misc Orofacial movements
topic_unstemmed	misc Dopamine D misc , D misc and D misc receptor subtypes misc Gα misc Gγ misc Adenylyl cyclase misc PKA misc DARPP-32 misc ‘Knockout’ misc Transgenic misc Behavioural phenotype misc Ethogram misc Orofacial movements
topic_browse	misc Dopamine D misc , D misc and D misc receptor subtypes misc Gα misc Gγ misc Adenylyl cyclase misc PKA misc DARPP-32 misc ‘Knockout’ misc Transgenic misc Behavioural phenotype misc Ethogram misc Orofacial movements
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title	Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
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title_full	Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
author_sort	Waddington, John L.
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author_browse	Waddington, John L. O'Tuathaigh, Colm O'Sullivan, Gerard Tomiyama, Katsunori Koshikawa, Noriaki Croke, David T.
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doi_str_mv	10.1007/s00213-005-0058-8
title_sort	phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
title_auth	Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
abstract	Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. © Springer-Verlag 2005
abstractGer	Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. © Springer-Verlag 2005
abstract_unstemmed	Background Mutants with targeted gene deletion (‘knockout’) or insertion (transgenic) of $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ dopamine (DA) receptor subtypes are complemented by an increasing variety of double knockout and transgenic-‘knockout’ models, together with knockout of critical components of DA receptor signalling cascades such as $ Gα_{olf} $[$ Gγ_{7} $], adenylyl cyclase type 5, PKA [RIIβ] and DARPP-32. However, it is increasingly recognised that these molecular techniques have a number of inherent limitations. Furthermore, there are poorly understood methodological factors that contribute to inconsistent phenotypic findings between laboratories. Objective This review seeks to document the impact of DA receptor subtype and related transduction mutants on our understanding of the behavioural roles of these entities, primarily at the level of unconditioned psychomotor behaviour. Methods It includes ethologically based and orofacial movement studies in our own laboratories, since these are the only studies to systematically compare each of the $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor and DARPP-32 signal transduction ‘knockouts’. Discussion There is a particular emphasis on identifying methodological factors that might influence phenotypic effects and account for inconsistencies. The findings are offered empirically to (1) specify the extent of phenotypic diversity among individual DA receptor subtypes and transduction components and (2) indicate relationships between $ D_{1} $, $ D_{2} $, $ D_{3} $, $ D_{4} $ and $ D_{5} $ receptor subtype proteins, associated $ Gα_{i} $/$ Gα_{s} $/$ Gα_{olf} $[$ Gγ_{7} $]–adenylyl cyclase type 5–PKA [RIIβ]–DARPP-32 signalling cascades and behaviour. The findings are also offered heuristically as a base for such phenotypic comparisons at additional levels of behaviour so that a yet more complete phenotypic profile might emerge. © Springer-Verlag 2005
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title_short	Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface
url	https://dx.doi.org/10.1007/s00213-005-0058-8
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up_date	2024-07-04T01:19:34.522Z
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Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology–molecular biology interface

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