Novel  MPDZ / MUPP1  transgenic and knockdown models confirm   Mpdz  's role in ethanol withdrawal and support its role in voluntary ethanol consumption | Zendy

Milner Lauren C. | Zendy; Shirley Renee L. | Zendy; Kozell Laura B. | Zendy; Walter Nicole A. | Zendy; Kruse Lauren C. | Zendy; Komiyama Noboru H. | Zendy; Grant Seth G. N. | Zendy; Buck Kari J. | Zendy

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Novel MPDZ / MUPP1 transgenic and knockdown models confirm Mpdz 's role in ethanol withdrawal and support its role in voluntary ethanol consumption

Author(s) -

Milner Lauren C.,

Shirley Renee L.,

Kozell Laura B.,

Walter Nicole A.,

Kruse Lauren C.,

Komiyama Noboru H.,

Grant Seth G. N.,

Buck Kari J.

Publication year - 2015

Publication title -

addiction biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.445

H-Index - 78

eISSN - 1369-1600

pISSN - 1355-6215

DOI - 10.1111/adb.12087

Subject(s) - knockout mouse , gene knockdown , genetically modified mouse , ethanol , transgene , heterozygote advantage , medicine , psychology , biology , endocrinology , gene , genetics , receptor , biochemistry , allele

Association studies implicate multiple PDZ domain protein ( MPDZ /MUPP1) sequence and/or expression in risk for alcoholism in humans and ethanol withdrawal ( EW ) in mice, but confirmation has been hindered by the dearth of targeted genetic models. We report the creation of transgenic ( MPDZ‐TG ) and knockout heterozygote ( Mpdz +/− ) mice, with increased (2.9‐fold) and decreased (53%) target expression, respectively. Both models differ in EW compared with wild‐type littermates ( P ≤ 0.03), providing compelling evidence for an inverse relationship between Mpdz expression and EW severity. Additionally, ethanol consumption is reduced up to 18% ( P = 0.006) in Mpdz +/− , providing the first evidence implicating Mpdz in ethanol self‐administration.

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