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Effect of maternal immune activation on progeny behavior in the Drd3‐EGFP mouse model
Author(s) -
Li Ying,
Kuzhikandathil Eldo
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb425
Subject(s) - offspring , dopaminergic , dopamine receptor , dopamine receptor d3 , prepulse inhibition , open field , dopamine , immune system , receptor , biology , dopamine receptor d2 , medicine , psychology , endocrinology , neuroscience , immunology , genetics , schizophrenia (object oriented programming) , psychiatry , pregnancy
Offspring of women who develop infections while pregnant are at a higher risk of developing mental disorders. Several rodent studies have shown that maternal immune activation (MIA) results in altered behavior in the progeny. The progeny also exhibit dopaminergic dysfunction which includes changes in D1 and D2 dopamine receptor expression. Among D2‐like receptors, the D3 dopamine receptor (D3R) has the highest affinity for dopamine and many commonly used antipsychotics. Our long‐term objective is to use the Drd3‐EGFP mouse model (which reports the endogenous expression of D3R) to determine the effect of MIA on D3R expression and function in the progeny. To this end, in this study, our objective was to use the Drd3‐EGFP mice strain to determine the effect of MIA on the behavior of the progeny. The viral mimic, Polyriboinosinic‐polyribocytidilic acid (PolyIC), was administered to pregnant Drd3‐EGFP mice to induce immune activation. The behavior of the resultant offspring was assessed in several tests. We found that 35‐ and 70‐day old offspring of maternally infected mothers showed increased anxiety in the Open Field test, reduced working memory in the Novel Object Recognition test, and exhibited prepulse inhibition deficits. These results validate the MIA experimental model in the Drd3‐EGFP mice and will facilitate studies that will examine changes in D3R expression and function. This research is supported by grants from NIH (MH82376) and the FM Kirby foundation.