2007 Annual Report 1a.Objectives (from AD-416) Improve the efficacy of diets to prevent clinical and subclinical hypocalcemia in the periparturient dairy cow. Use of genomic and proteomic approaches to identify genes in the kidney, intestine, and/or mammary gland that are modulated by vitamin D metabolites and dietary cation-anion difference (DCAD) diets to better understand the molecular basis of disease and develop effective intervention strategies to prevent hypocalcemia in the transition cow. Identify the pathways (genes/proteins) responsible for calcium entry, calcium storage, and calcium transport in the mammary gland as well as points of regulation for these calcium transport and storage mechanisms. Determine primary factors responsible for excess mammary calcium drain in animals with hypocalcemia. 1b.Approach (from AD-416) The approach to this research is a combination of applied and basic investigations to obtain new knowledge that will increase understanding and result in practical solutions for the prevention of subclinical a clinical hypocalcemia in dairy cows. The research will investigate the mechanism of action of DCAD diets in the prevention of hypocalcemia. Agronomic research will be used to develop forages that are low in DCAD thus providing more palatable approaches to feeding low DCAD diets for prevention of hypocalcemia. Basic research approaches will be employed to gain an understanding of role and contribution of mammary calcium transport in the development of clinical and subclinical hypocalcemia in cows. 4.Accomplishments Calcium Homeostasis in the Transition Cow: Calcium loss through the mammary gland contributes to milk fever and immune suppression in the periparturient cow. These disease complications adversely affect the dairy producer’s profitability. A mammary gland calcium pump named SPCA1, was thought to be the second most abundant Ca2+-ATPase found in lactating mammary tissue. SPCA1 was also the only mammary calcium pump to show increased protein expression prepartum, thus supporting the hypothesis that the SPCA1 is likely responsible for pumping calcium into the mammary gland in advance of lactation. The amount of SPCA1 in the prepartum mammary gland was found to be significantly higher in cows that would go on to develop clinical hypocalcemia (milk fever), suggesting that more rapid filling of the mammary calcium pool prepartum may contribute to a cow’s hypocalcemia. We have new data that shows that the newly discovered calcium pump, which is, named SPCA2, parallels many of our findings with regard to SPCA1. This second SPCA calcium pump will help us unravel the role of these unique calcium pumps in the development of milk fever and hypocalcemia-related immunosuppression. The impact of this data is a greater understanding of the role that the mammary gland plays in the development of milk fever in cows and how the mammary gland regulates calcium needs of the immune system. Therefore, we will be able to understand and possibly control immune suppression in transition cows which will benefit cow health, and therefore farm profitability. This research is part of the Animal Health National Program 103, Component 5: Countermeasures to Prevent and Control Reproductive and Neonatal Diseases, of the Animal Health Action Plan. 5.Significant Activities that Support Special Target Populations None.