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J Neurosci DOI:10.1523/JNEUROSCI.0229-12.2012

Strain-specific regulation of striatal phenotype in Drd2-eGFP BAC transgenic mice.

Publication TypeJournal Article
Year of Publication2012
AuthorsC Chan, S, Peterson, JD, Gertler, TS, Glajch, KE, Quintana, RE, Cui, Q, Sebel, LE, Plotkin, JL, Shen, W, Heiman, M, Heintz, N, Greengard, P, D Surmeier, J
JournalJ Neurosci
Volume32
Issue27
Pages9124-32
Date Published2012 Jul 04
ISSN1529-2401
KeywordsAnimals, Animals, Outbred Strains, Basal Ganglia Diseases, Behavior, Animal, Chromosomes, Artificial, Bacterial, Corpus Striatum, Disease Models, Animal, Female, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Hemizygote, Male, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Transgenic, Motor Activity, Phenotype, Receptors, Dopamine D2, Species Specificity
Abstract

Mice carrying bacterial artificial chromosome (BAC) transgenes have become important tools for neuroscientists, providing a powerful means of dissecting complex neural circuits in the brain. Recently, it was reported that one popular line of these mice--mice possessing a BAC transgene with a D(2) dopamine receptor (Drd2) promoter construct coupled to an enhanced green fluorescent protein (eGFP) reporter--had abnormal striatal gene expression, physiology, and motor behavior. Unlike most of the work using BAC mice, this interesting study relied upon mice backcrossed on the outbred Swiss Webster (SW) strain that were homozygous for the Drd2-eGFP BAC transgene. The experiments reported here were conducted to determine whether mouse strain or zygosity was a factor in the reported abnormalities. As reported, SW mice were very sensitive to transgene expression. However, in more commonly used inbred strains of mice (C57BL/6, FVB/N) that were hemizygous for the transgene, the Drd2-eGFP BAC transgene did not alter striatal gene expression, physiology, or motor behavior. Thus, the use of inbred strains of mice that are hemizygous for the Drd2 BAC transgene provides a reliable tool for studying basal ganglia function.

URLhttp://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=22764222
DOI10.1523/JNEUROSCI.0229-12.2012
Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/22764222?dopt=Abstract

Alternate JournalJ. Neurosci.
PubMed ID22764222
PubMed Central IDPMC3461272
Grant ListR01 NS034696 / NS / NINDS NIH HHS / United States
NS069777 / NS / NINDS NIH HHS / United States
R01 NS069777 / NS / NINDS NIH HHS / United States
NS34696 / NS / NINDS NIH HHS / United States
NS069777-S1 / NS / NINDS NIH HHS / United States
R37 NS034696 / NS / NINDS NIH HHS / United States