The model we use for this experiment is WT mice with ERα intact in kisspeptin neurons, and KERKO mice where ERα is knocked out in kisspeptin neurons.
Then the researchers compare various features between WT mice and the knock-out mice 1. The first factor they compared between KERKO and WT mice is how is the presence /absence of the ERα affects the onset of puberty * We predict that the puberty onset for the KERKO mice will be dramatically advanced due to the ablation of ERα in kisspeptin neurons. * We are going to look at this factor by comparing 1. Age at vaginal opening between the WT and KERKO mice (advanced in KERKO) 2. Serum LH levels … (LH level abnormally elevated in prepubertal KERKO mice) KERKO mice exhibit premature activation of the reproductive axis. 2. The second factor to compare is whether normal estrous cycle is developed in WT and KERKO mice * Shows that KERKO mice fail to develop normal estrous cyclicity * Ovarian Histology… , * abundance of CL are present in WT mice, which are absent in KERKO mice comfirm anovulation associated with the observed estrous acyclicity * these findings reveal that KERKO mice do not acquire the capacity to sustain normal ovulatory cyclicity, and hence fail to fully progress through puberty 3. The next factor we are going to look at is the kisspeptin expression at hypothalamic arcuate nucleus (ARC) neurons ---“inhibitory effects” and anteroventral periventricular (AVPe) neurons ---“stimulatory actions” * Immnunohistochemical labeling of kisspeptin cells in the AVPe and ARC of WT and KERKO mice shows that Kisspeptin expression fails to develop normally in AVPe of KERKO mice (A and B), but the expression is increased in ARC neurons in KERKO 4. The last factor to compare is