Literature DB >> 27558735

The Impact of Oxytocin Gene Knockout on Sexual Behavior and Gene Expression Related to Neuroendocrine Systems in the Brain of Female Mice.

Josi Maria Zimmermann-Peruzatto1, Virgínia Meneghini Lazzari2, Grasiela Agnes2, Roberta Oriques Becker2, Ana Carolina de Moura2, Renata Padilha Guedes2, Aldo Bolten Lucion1, Silvana Almeida2,3, Márcia Giovenardi4,5,6.   

Abstract

Social relations are built and maintained from the interaction among individuals. The oxytocin (OT), vasopressin (VP), estrogen, dopamine, and their receptors are involved in the modulation of sexual behavior in females. This study aimed to analyze the impact of OT gene knockout (OTKO) on sexual behavior and the gene expression of oxytocin (OTR), estrogen alpha (ERα), estrogen beta (ERβ), vasopressin (V1aR), and dopamine (D2R) receptors in the olfactory bulb (OB), prefrontal cortex (PFC), hippocampus (HPC), and hypothalamus (HPT), as well as in the synthesis of VP in the HPT of female mice. Wild-type (WT) littermates were used for comparisons. The CDNAs were synthesized by polymerase chain reaction and the gene expression was calculated with the 2-ΔΔCt formula. Our results showed that the absence of OT caused an increase in the frequency and duration of non-receptive postures and a decrease in receptive postures in the OTKO. OTKO females showed a significant decrease in the gene expression of OTR in the HPC, V1aR in the HPT, and ERα and ERβ in the PFC. There was no significant difference in the gene expression of D2R of OTKO. However, OTKO showed an increased gene expression of V1aR in the HPC. There is no significant difference in VP mRNA synthesis in the HPT between OTKO and WT. Our findings demonstrate that the absence of OT leads to significant changes in the expression of the studied genes (OTR, ERα, ERβ, V1aR), and these changes may contribute to the decreased sexual behavior observed in OTKO females.

Entities:  

Keywords:  Dopamine; Estrogens; Female sexual behavior; OTKO; Vasopressin

Mesh:

Substances:

Year:  2016        PMID: 27558735     DOI: 10.1007/s10571-016-0419-3

Source DB:  PubMed          Journal:  Cell Mol Neurobiol        ISSN: 0272-4340            Impact factor:   5.046


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