Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. II. Impaired maturation of Purkinje cells.

Zinc deficiency during the first 3 postnatal weeks retarded the maturation of Purkinje cells. The dendrites of the Purkinje cells of 21-day-old zinc-deficient (ZD) rats were reduced in size and had fewer branches. Somatic processes were found in 24% of the Purkinje cells of ZD animals. Only 3% of the Purkinje cells of normal animals had somatic processes. A basal polysomal mass in the Purkinje cells of 21-day-old ZD rats indicated that zinc deficiency impaired the cytoplasmic maturation of Purkinje cells. The development of the glial envestment of the dendrites and the maturation of climbing fibers also were retarded. Pair-fed controls were studied to control for the effects of inanition in the ZD dams. In the pups of pair-fed dams, undernutrition slightly impaired the growth of the dendrites but produced few qualitative changes in the maturation of the soma and climbing fibers. Somatic processes were found on 10% of the Purkinje cells of pair-fed animals. Thus, the findings in the ZD animals were not only caused by the decreased maternal food consumption but by zinc deficiency. The retarded maturation of Purkinje cells was related to the altered metabolism of Purkinje cells and to effects secondary to decreased numbers of parallel fibers.

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

The effects of zinc deficiency on cerebellar development were investigated in suckling rats. In 21-day-old zinc-deficient rats the cerebellum as well as the whole brain was reduced in size. The cerebellar cortex was underdeveloped and showed a persistence of the external granule cell layer, a reduction in the thickness of molecular layer and a decrease in the area of the internal granule cell layer. Lobular variations were present. Along the posterior superior fissure there was approximately a 60% reduction in the number of granule cells and in the number of granule cells per Purkinje cell. It was suggested that the reduction in the number of granule cells was predominantly the result of impaired cell proliferation in the external granule cell layer. Comparisons with undernourished, pair-fed pups indicated that the effects of zinc deficiency could not be mediated totally through the reduced food consumption experienced by zinc deficient dams.

Morphology of the perforating cartilage canals in the proximal tibial growth plate of the chick.

Perforating canals arise exclusively from junctional canals just above the reserve zone and they do not branch after entering the proliferative zone. They are uniformly spaced and arranged in parallel array. The cartilage canals terminate near the beginning of the zone of hypertrophic cartilage cells. Vascular components within the perforating canals consist of a central arteriole surrounded by enlarged, interconnected capillaries which are individually in contact with the adjacent cartilage matrix. TEM shows that the capillary endothelium is extremely attenuated, possesses numerous fenestrations and lacks a continuous basement membrane. The central arteriole is enlarged through the midpart of the canal and then narrows to communicate with the capillaries near the bottom of the canal. The large capillaries ascend from their point of origin and recombine near the top of the growth plate to exit as a single venule. The vascular arrangement therefore describes a system in which the outgoing blood runs in close proximity, but counter to, the incoming blood. This vascular arrangement within the perforating cartilage canal would most likely allow the zone of maturing cartilage cells to receive the highest concentration of nutrients.

Nickel deficiency and nickel-rhodium interaction in chicks.

Nickel deficiency was produced in chicks under near optimal growth conditions. This judgment is based on the finding that chicks fed the experimental diet supplemented with nickel had a very satisfactory growth rate, over 600 g in 4 weeks. To induce nickel deficiency, chicks were raised in plastic cages located inside plastic isolators and were fed diets (containing 2-15 ng of nickel/g) based on dried skim milk, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. In 2 experiments, controls were fed 3 mug of nickel/g as NiCl2-6H2O. In experiment 3, instead of 1 control group 25, 50, 250, and 2,500 ng/g of supplemental dietary nickel as NiCl2-6H2O were each given to separate groups of chicks. Nickel deprivation resulted in: ultrastructural changes in the liver with the most obvious abnormality in the organization of the rough endoplasmic reticulum; altered gross appearance, reduced oxidative ability, and decreased lipid phosphorus in the liver; altered shank skin pigmentation that was associated with a decrease in yellow lipochrome pigments; and lower hematocrits. Deficiency also tended to increase the thickness of the legs and size of the hock; decrease the length:width ratios of the tibias and femurs; and decrease the plasma cholesterol. None of the signs of deficiency were seen in chicks fed diets containing at least 52 ng of nickel/g. In one experiment, a group of birds was fed 50 mug of rhodium/g of diet as (ClRh(NH3)5)SO4 to ascertain whether rhodium is a metabolic antagonist of nickel. Supplemental rhodium increased the hematocrits and liver oxidative ability of both nickel-deficient and -supplemented chicks, and increased total liver lipids, liver lipid phosphorus, and liver cholesterol in the nickel-deficient chicks alone. Rhodium did not increase the signs of nickel deficiency.

Nickel deficiency in rats.

Nickel deficiency was produced in rats fed diet (containing 2-15 ng of mickel/g) based on dried skim mile, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. Controls were fed a supplemental 3 mug of nickel/g of diet as NiCl2-6H2O. The rats were raised in plastic cages located inside laminar flow racks. Nickel deprivation resulted in several consistent pathological findings. These included: (1) increased perinatal mortality, (2) unthriftiness in young rats characterized by a rough coat and/or uneven hair development, (3) altered gross appearance (color) of the liver, (4) increased rate of alpha-glycerophosphate oxidation by liver homogenates, (5) decreased liver cholesterol, and (6) ultrastructural changes in the liver with the most obvious difference in the amount and organization of the rough endoplasmic reticulum. Nickel deficiency in rats tended to decrease growth, hematocrits, and liver total lipids and phospholipids.