Remodeling of mammary tissue and lactation persistency

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The long range objective of this research program is to develop an economically viable and consumer acceptable technology that would improve lactation persistency and enable longer lactation in dairy cows. From a mammary gland perspective, milk production is simply a function of the number of secretory cells and the secretory activity of these cells.  In goats,   it is the loss of secretory cells which accounts for the decrease in milk yield during declining lactation.  It is now well established in rodents and ruminants that mammary cell loss during involution (termination of lactation) occurs through programmed cell death (apoptosis).  Apoptosis also occurs in late lactation and accounts for the progressive loss of secretory cells in declining lactation.  Therefore, there are considerable incentives to identify the factors that regulate mammary apoptosis, in particular during these early stages of gradual involution.My hypotheses are:-It is possible to reduce the rate of decline in milk production by reducing the rate of mammary cell death;-The milking-induced PRL release is important to maintain the differentiation and the survival of the mammary epithelial cells;-Stanniocalcin reduces intracellular level of Ca2+ which reduce synthesis of milk component.My short range objectives are:1- To evaluate apoptosis, cell proliferation and expression of STC in cows with different rates of lactation decline. Factors affecting rate of  lactation decline will be parity, pregnancy and feed restriction.  2- To determine the role of calcium homeostasis in the control of mammary gland functions 3- To determine the role of milking induce release of prolactin on lactation persistency. Rate of lactation decline, gene expression, and cell apoptosis will be evaluated in cows where prolactin release will be prevented during 8 weeks by administration of an inhibitor of prolactin release.4- To determine the factors controling the magnitude of milking-induced release of prolactin