Some of the material in is restricted to members of the community. By logging in, you may be able to gain additional access to certain collections or items. If you have questions about access or logging in, please use the form on the Contact Page.
The focus of this work is pulsatile prolactin (PRL) secretion, which includes in vivo experiments on PRL release in female rats and mathematical modeling at the system and single-cell level . First we investigate the generation of the semicircadian rhythm of PRL that occurs during the first half of pregnancy in female rats. Using an experimental approach we show that this rhythm can be induced by the injection of oxytocin, suggesting that this hormone is responsible for triggering the rhythm. Using mathematical modeling, we propose a likely mechanism for this effect. According to this model, the PRL rhythm is generated by the interaction of hypothalamic neurons and pituitary lactotrophs. In the second part of this work we study PRL release on the single-cell level. First we develop a mathematical model of the pituitary lactotroph and use it to identify the mechanism for the stimulatory effects of dopamine (DA) on lactotrophs. These effects are paradoxical since DA activates only inhibitory ionic currents. We also show cases of bursting in the absence of a slow variable and analyze the dynamic mechanism for this novel form of bursting. Finally, we develop a mathematical model of the effect of endothelin (ET) on PRL secretion from pituitary lactotrophs. This model combines four different biochemical signaling pathways, each of which is activated by ET and mediated by G-proteins.