Literature DB >> 12865890

Topographical Assessment of Ethological and Dopamine Receptor Agonist-Induced Behavioral Phenotype in Mutants with Congenic DARPP-32 'Knockout'.

Rachel E Nally1, Fergal N McNamara, Jeremiah J Clifford, A Kinsella, Orna Tighe, David T Croke, Allen A Fienberg, Paul Greengard, John L Waddington.   

Abstract

Congenic (10 backcrosses into C57BL/6J) mutants with targeted gene deletion of DARPP-32, a neuronal phosphoprotein regarded as an essential mediator of the biological effects of dopamine (DA), were assessed phenotypically using an ethologically based approach that resolves all topographies of behavior in the mouse repertoire. Over initial exploration, female, but not male, DARPP-32 mutants evidenced increased locomotion and decreased grooming, while a decrease in rearing seated was evident in mutants of both genders; continuing assessment over several hours did not reveal additional phenotypic effects. Following challenge with the nonselective DA receptor agonist apomorphine, low doses were associated with reduced levels of sniffing, grooming, total rearing, and rearing seated in DARPP-32 mutants relative to wildtypes; this would suggest some role for DARPP-32 in mediating the biological effects of presynaptic D(2)-like autoreceptor or inhibitory postsynaptic D(2)-like receptor activation. Following challenge with higher doses, while stereotyped sniffing and locomotion with chewing was largely unaltered, the additional murine response of Straub tail was essentially abolished in DARPP-32 mutants, indicating some specific involvement of DARPP-32 in mediating this topography of behavior; additionally, there were overall reductions in levels of sniffing, total rearing, rearing seated, and grooming in DARPP-32 mutants that were unrelated to the dose of apomorphine administered, indicating broader topographical effects following the stress of the injection procedure relative to more naturalistic conditions. The developmental absence of DARPP-32 following targeted gene deletion appears to be associated with compensatory processes that maintain certain topographies of spontaneous and agonist-induced DAergic function, while other topographies remain impaired.

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Year:  2003        PMID: 12865890     DOI: 10.1038/sj.npp.1300259

Source DB:  PubMed          Journal:  Neuropsychopharmacology        ISSN: 0893-133X            Impact factor:   7.853


  3 in total

Review 1.  Phenotypic studies on dopamine receptor subtype and associated signal transduction mutants: insights and challenges from 10 years at the psychopharmacology-molecular biology interface.

Authors:  John L Waddington; Colm O'Tuathaigh; Gerard O'Sullivan; Katsunori Tomiyama; Noriaki Koshikawa; David T Croke
Journal:  Psychopharmacology (Berl)       Date:  2005-09-29       Impact factor: 4.530

2.  Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior.

Authors:  Ilse Gantois; Ke Fang; Luning Jiang; Daniela Babovic; Andrew J Lawrence; Vincenzo Ferreri; Yaroslav Teper; Bianca Jupp; Jenna Ziebell; Cristina M Morganti-Kossmann; Terence J O'Brien; Rachel Nally; Günter Schütz; John Waddington; Gary F Egan; John Drago
Journal:  Proc Natl Acad Sci U S A       Date:  2007-02-28       Impact factor: 11.205

3.  D1 dopamine receptor coupling to PLCβ regulates forward locomotion in mice.

Authors:  Ivan O Medvedev; Amy J Ramsey; Shababa T Masoud; Marie Kristel Bermejo; Nikhil Urs; Tatyana D Sotnikova; Jean-Martin Beaulieu; Raul R Gainetdinov; Ali Salahpour
Journal:  J Neurosci       Date:  2013-11-13       Impact factor: 6.167

  3 in total

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