| First Author | Götz V | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 6 | Pages | 112543 |
| PubMed ID | 37224016 | Mgi Jnum | J:359534 |
| Mgi Id | MGI:7787276 | Doi | 10.1016/j.celrep.2023.112543 |
| Citation | Gotz V, et al. (2023) Ovulation is triggered by a cyclical modulation of gonadotropes into a hyperexcitable state. Cell Rep 42(6):112543 |
| abstractText | Gonadotropes in the anterior pituitary gland are essential for fertility and provide a functional link between the brain and the gonads. To trigger ovulation, gonadotrope cells release massive amounts of luteinizing hormone (LH). The mechanism underlying this remains unclear. Here, we utilize a mouse model expressing a genetically encoded Ca(2+) indicator exclusively in gonadotropes to dissect this mechanism in intact pituitaries. We demonstrate that female gonadotropes exclusively exhibit a state of hyperexcitability during the LH surge, resulting in spontaneous [Ca(2+)](i) transients in these cells, which persist in the absence of any in vivo hormonal signals. L-type Ca(2+) channels and transient receptor potential channel A1 (TRPA1) together with intracellular reactive oxygen species (ROS) levels ensure this state of hyperexcitability. Consistent with this, virus-assisted triple knockout of Trpa1 and L-type Ca(2+) subunits in gonadotropes leads to vaginal closure in cycling females. Our data provide insight into molecular mechanisms required for ovulation and reproductive success in mammals. |
