Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. I. Impaired acquisition of granule cells

Dvergsten, Christopher L.; Fosmire, Gary J.; Ollerich, Dwayne A.; Sandstead, Harold H.

doi:10.1016/0006-8993(83)90284-6

Cited by 82 publications

(37 citation statements)

References 39 publications

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“…Similarly impairments in learning and memory impairment were observed in adult rats whose mothers were subjected to severe zinc deficiency during pregnancy and lactation [9], [10]. Histological abnormalities were evident in the cerebellum and hippocampus in rats with late prenatal and/or early postnatal zinc deficiency [6][7][8], [25], [26]. Severe zinc deficiency imposed throughout pregnancy by with diets containing less than 1 mg Zn/kg/day resulted in gross anatomaical abnormalities in offspring.…”

Section: Discussionmentioning

confidence: 98%

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Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

et al. 2001

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Effects of maternal dietary zinc deficiency on prenatal and postnatal brain development were investigated in ICR strain mice. From d 1 of pregnancy (E0) until postnatal d 20 (P20), maternal mice were fed experimental diets that contained 1 mg Zn/kg/day (severe zinc deficient, SZD), 5 mg Zn/kg/day (marginal zinc deficient, MZD), 30 mg Zn/kg/day (zinc adequately supplied, ZA) or 100 mg Zn/kg/day (zinc supplemented, ZS and pair-fed, PF). Brains of offspring from these dietary groups were examined at various developmental stages for expression of nestin, an intermediate filament protein found in neural stem cells and young neurons. Immunocytochemistry showed nestin expression in neural tube 10.5 d post citrus (dpc) as well as in the cerebral cortex and neural tube from 10.5 dpc to postnatal d 10 (P10). Nestin immunoreactivities in both brain and neural tube of those zinc-supplemented control groups (ZA, ZS, PF) were stronger than those in zinc-deficient groups (SZD and MZD). Western blot analysis confirmed that nestin levels in pooled brain extracts from each of the zinc-supplemented groups (ZA, ZS, PF) were much higher than those from the zinc-deficient groups (SZD and MZD) from 10.5 dpc to P10. Immunostaining and Western blots showed no detectable nestin in any of the experimental and control group brains after P20. These observations of an association between maternal zinc deficiency and decreased nestin protein levels in brains of offspring suggest that zinc deficiency suppresses development of neural stem cells, an effect which may lead to neuroanatomical and behavioral abnormalities in adults.

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Section: Discussionmentioning

confidence: 98%

“…development [2], [4], [5]. Dvergsten et al [6][7][8] investigated the effects of maternal zinc deficiency on postnatal development of the rat cerebellar cortex. Granule cell neurons were sharply reduced in cell number, Purkinje cell maturation was impaired, and differentiation of basket and stellate cell dendrites was reduced.…”

Section: Introductionmentioning

confidence: 99%

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

et al. 2001

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“…Incorporation of thymidine into DNA was suppressed in 10-day-old sucklings (334). Histologic examination of the cerebellum on the 21st postnatal day found retarded maturation (335) and impaired division and migration of external granular cell neurons (336,337). In addition the arborization of Purkinje, stellate and basket cell dendrites was decreased and morphologically grossly abnormal; the number of boutons was decreased and their shapes were strikingly abnormal (336,337).…”

Section: Importance Of Zinc To Brain Devel-opment and Function: Animamentioning

confidence: 92%

Zinc: Health Effects and Research Priorities for the 1990s

Walsh¹,

Sandstead²,

Prasad³

et al. 1994

Environmental Health Perspectives

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This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level. - There is considerable evidence that zinc deficiency in humans is a serious worldwide problem and outweighs the potential problem of accidental, self-imposed, or environmental exposure to zinc excess. Acute deficiency (1) and chronic deficiency (2) are well-known entities in human populations and are probably much more common than generally recognized. The importance of zinc for human health was first documented in 1963 (3) Telephone (617) (617) 638-4329. E-mail: ctwalsh~bu.edu renal disease, and other chronically debilitating diseases are now known to be predisposing factors for zinc deficiency in humans (4).Zinc deficiency is reflected in clinical syndromes which affect men and women of all ages and all socioeconomic and cultural classes in the United States. It is neither prevalent in any specific area of the United States nor associated with any specific or definitive biochemical marker, which can make its identification difficult and confusing. Its presence is manifested by a wide spectrum of symptoms, from acute, life threatening problems to mild subclinical or marginal disorders which may only vaguely disturb well being. The acute problems are often seen in profoundly ill patients treated in hospitals, whereas subclinical problems may be so vague that patients seek assistance outside traditional medical practice.Based upon clinical data and using traditional, epidemiologic techniques, Henkin and Aamodt (5) have reclassified zinc deficiency into three syndromes; these are a) acute, b) chronic, and c) subacute zinc deficiency. Acute zinc deficiency is relatively uncommon and follows parenteral hyperalimentation or oral L-histidine administration. Chronic zinc deficiency is more common, usually resulting from chronic dietary lack of zinc. Subacute or latent zinc deficiency is the most common of these syndromes. It is estimated that there are 4...

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“…Zinc can play a central role in neuronal proliferation, differentiation, and migration, and also regulating apoptotic neuronal death (Dvergsten et al, 1983(Dvergsten et al, , 1984aVerstraeten et al, 2004). A decrease in neuronal zinc leads to an increase in cellular oxidants.…”

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confidence: 99%

Zinc and the cytoskeleton in the neuronal modulation of transcription factor NFAT

Mackenzie

Oteiza

2006

Journal Cellular Physiology

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Transcription factor NFAT is crucial in the development of the nervous system due to its role in neuronal plasticity and survival. In this study we characterized the role of zinc and the cytoskeleton in the modulation of NFAT in neuronal cells. The incubation of cells in zinc deficient media led to NFAT activation that was inhibited by the calcium chelator BAPTA and the antioxidants (AE)-a-lipoic acid and N-acetyl cysteine, suggesting the involvement of calcium and oxidants in the initial steps of NFAT activation associated with zinc deficiency. At a second step of regulation, a decrease in cellular zinc led to an impaired transport of the active NFAT from the cytosol into the nucleus due to alterations in tubulin polymerization secondary to a decrease in neuronal zinc. Furthermore, disruption of the cytoskeleton structure by cold and chemical agents (colchicine (Col), vinblastine (VB), cytochalasin D (Cyt)) also inhibited NFAT transport into the nucleus. The altered nuclear transport caused a decrease in NFAT-dependent gene expression. This study demonstrates for the first time that zinc can modulate transcription factor NFAT in neuronal cells, and that microtubules are involved in NFAT nuclear translocation, crucial event in the regulation of NFAT transcriptional activity.

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Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. I. Impaired acquisition of granule cells

Cited by 82 publications

References 39 publications

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

Zinc: Health Effects and Research Priorities for the 1990s

Zinc and the cytoskeleton in the neuronal modulation of transcription factor NFAT

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