Maternal zinc deficiency reduces NMDA receptor expression in neonatal rat brain, which persists into early adulthood

• DOI: 10.1111/j.1471-4159.2005.03246.x
• Publication Date: 2005-06-30T17:28:20Z
• Authors: Winyoo Chowanadisai; Shannon L. Kelleher; Bo Lönnerdal
• Keywords: Early adulthood

Abstract Prenatal and early postnatal zinc deficiency impairs learning memory these deficits persist into adulthood. A key modulator in this process may be the NMDA receptor; however, effects of on regulation receptor activity are not well understood. Female Sprague‐Dawley rats were fed diets containing 7 (zinc deficient, ZD), 10 (marginally MZD) or 25 (control) mg Zn/g diet preconception through day (PN) 20, at which time pups weaned onto their maternal control diet. Regulation expression was examined PN2, PN11, PN65. At whole brain subunits NR1, NR2A, NR2B lower from dams ZD MZD compared to controls, as analyzed using relative RT–PCR immunoblotting. hippocampi PSA‐NCAM (polysialic acid–neural cell adhesion molecule) number immunoreactive cells controls. Whole brain‐derived neurotrophic factor (BDNF) nerve growth (NGF) concentrations both low diets, respectively. NR1 remained previously zinc‐deficient These data indicate potential mechanisms developmental can impair later life.