Abstract
Effects of prenatal and postnatal zinc deficiency on the composition of the brain and on subsequent adult behavior were studied. Deficiency throughout the latter third of pregnancy resulted in decreased body and brain size without affecting total brain DNA, RNA, or protein. Adult males that had been subjected to intrauterine zinc deficiency displayed impaired shock avoidance. Zinc deficiency from birth until 21 days of age resulted in impaired growth, decreased brain size, diminished brain DNA, RNA and protein. Cerebellar lipid concentration was also diminished. Such male animals displayed impaired maze acquisition as adults.—Sandstead, H. H., G. J. Fosmire, J. M. McKenzie and E. S. Halas. Zinc deficiency and brain development in the rat. Federation Proc. 34: 86–88, 1975.
From Session IV, Aging of homeostatic control systems, of the FASEB Conference on Biology of Development and Aging, presented at the 58th Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, N. J., April 10, 1974.
Supported in part by the USDA Cooperative Agreement 12-14-100-11, 178 (61), Amend. 1.
Public Health Service, International Research Fellow.
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Sandstead, H.H., Fosmire, G.J., McKenzie, J.M., Halas, E.S. (1975). Zinc deficiency and brain development in the rat. In: Thorbecke, G.J. (eds) Biology of Aging and Development. Faseb Monographs, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2631-1_19
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