Possible involvement of transient receptor potential channels in adenomyosis
To investigate the role and mechanism of the TRPM3 antagonist, primidone in tamoxifen-induced adenomyosis mouse. The neonatal female mice were randomly divided into three groups: control group, adenomyosis group and primidone treatment group. We then performed gene expression profiling analysis using data obtained from RNA-seq of uterus from different groups Overall design: The neonatal female mice were randomly divided into three groups: control group, adenomyosis group and primidone treatment group. From day 1 to day 5 after birth, female neonatal mice in the ADE group (n=3) and primidone treatment group (n=3) received 1 mg/kg tamoxifen suspended in a peanut oil/lecithin/condensed milk mixture (2:0.2:3, by volume) at a dose volume of 5 µl/g body weight, while the control neonatal mice (n=3) were fed similarly with the same amount of solvent without tamoxifen. All mice were weaned and separated from the dams upon reaching 3 weeks of age, where the dams were sacrificed using cervical dislocation. From 10 weeks after birth, mice in primidone treatment group were administered by intraperitoneal injection with either primidone (2mg/kg/d) for 3 weeks, while the mice in the control and ADE groups were administered similarly with corresponding quantities of the vehicle.  Uterine samples from the mice in different group were harvested at 13 weeks of age for RNA-seq.