Nitric oxide synthase system in the brain development of neonatal hypothyroid rats.

Thyroid hormones play an important morphogenetic role during the fetal and neonatal periods and regulate numerous metabolic processes. In the central nervous system, they control myelination and overall brain development, regional gene expression, and regulation of oxygen consumption. Their deficiency in the fetal and neonatal periods causes severe mental retardation, due to lack of thyroid function, or to iodine deficiency.

Movement activity recovers the loss of spines owing to chronic immobilization.

In chronically movement-restricted Wistar rats, we described a significant decrease of spines along apical shafts of layer V cortical pyramids. Current study indicates that the liberation at 40 days of rats whose movements had been restricted since 20 days of age produces a gradual recovery of the number of spines, reaching the control values at 80 days of age and that this process occurred faster in the motor than in the sensory cortices. Nevertheless, when R(20) rats were liberated at 80 days, the number of spines had not fully recovered when rats were 120 days old.

Movements restriction and alterations of the number of spines distributed along the apical shafts of layer V pyramids in motor and primary sensory cortices of the peripubertal and adult rat.

The number and distribution of spines along apical shafts of rapid-Golgi-stained layer V pyramidal cells from visual, motor and somatosensory cortical areas were analyzed in control and movement-restricted (beginning at 20 days old) Wistar rats killed at 30, 40, 80 and 120 days of age (experiment A). In other group of rats, spine density was analyzed when restriction initiates on day 40 and the animals were killed at 50, 60 and 80 days postpartum, or after restriction starting on day 80 and killed at 120 days of age (experiment B). It has been found that the restriction of movements significantly reduces the total number of spines on apical shafts in the three cortical areas, when this condition starts at 20, 40 or 80 days without changing the overall distribution of spines.

Hypothyroidism alters the development of radial glial cells in the term fetal and postnatal neocortex of the rat.

Alterations of thyroid function during human development are known to produce extensive damage to the central nervous system including severe mental retardation. Using immunohistochemistry to identify the intermediate filament nestin, we have studied the possible influence of fetal and neonatal hypothyroidism on neocortical neuronal migration by arresting the normal development of the radial glial scaffold. By embryonic day 21 (E21), hypothyroid animals had a significant decrease in the number of nestin immunoreactive processes in the presumptive visual cortex.

Neonatal food restriction induces hypoplasia in developing facial motor neurons of rats.

The effects of neonatal food restriction upon the dendritic development of facial nucleus (FN) motor neurons of Wistar rats were analyzed. Rats neonatally underfed by daily (12 h) mother-litter separation in an incubator from 5-30 days after birth exhibited, in brain stem Golgi-Cox sections, significant reductions in the number and extension of stellate, triangular and bipolar FN neuronal dendritic prolongations with negligible effects upon perikarya measurements. Data suggest that in the underfed newborn, the ability of FN neurons to establish synaptic contacts with afferent fibers is reduced, which then interferes with their capacities for the integration and triggering of nerve impulses to modulate facial motor expression in response to sensory cues.