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February 1976

Hypomyelination in Copper-Deficient Rats: Prenatal and Postnatal Copper Replacement

Author Affiliations

From the Developmental and Metabolic Neurology Branch, National Institute of Neurological Diseases and Stroke, Bethesda, Md (Drs Zimmerman, Matthieu, Quarles, and Brady), and the Veterans Administration Hospital, Baltimore (Dr Hsu). Dr Zimmerman is now with the Department of Neurology, Johns Hopkins Hospital, Baltimore; Dr Matthieu is now with the Service de Pédiatrie, Hôpital Cantonal Universitaire, Lausanne, Switzerland.

Arch Neurol. 1976;33(2):111-119. doi:10.1001/archneur.1976.00500020039007

• Copper deficiency induced by a low copper diet in three generations of rats was associated with substantial reductions in the yield of myelin (56%), brain weight (11%), and body weight (43%) in F2 generation rat pups nursed by their own copper-deficient mothers. The composition of the purified myelin was not different from that of controls in the content of individual proteins, lipids, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) activity, or GM1 ganglioside. The major myelin-associated glycoprotein (mGP) was consistently shifted slightly toward higher apparent molecular weight in the copper-deficient animals. Postnatal copper replacement by a foster mother produced a normal yield of myelin per gram of brain tissue, but failed to reverse the deficiency of brain and body growth. After copper replacement in a copper-deficient mother's diet prior to conception, a subsequent litter showed correction of all abnormalities found in her previous litters. The results suggest that copper is essential for myelin formation and general growth during critical periods in development.