Neuronal development in vitamin B6 deficiency

Abstract

The morphological changes observed in developing brain regions associated with maternal vitamin B6 deficits are summarized in Table 4. Brain development is a complex and orderly process consisting of cell division, proliferation, migration, and maturation. In the rat, vitamin B6 deficits imposed in utero and up to 30 days postnatal interfere with this orderly process. Deficits of the vitamin imposed in utero have been associated with reduced numbers of total and normal neurons in neocortex and with increased shrunken neurons (700-1500% of controls) in this region. These changes reflect the critical role of vitamin B6 in both neurogenesis and neuron longevity in neocortex. Postnatal cellular events in the neocortex, that is, neuron differentiation and synaptogenesis, were also altered by vitamin B6 deficits; higher order dendrites were reduced on stellate neurons in Layer II and on pyramidal neurons in Layer V. Synaptic density was less in the neutrophil of neocortex and in caudate/putamen, but structural integrity of the synapse was maintained. In cerebellum, both the molecular and granular areas were reduced, the monolayer organization of Purkinje cells was disrupted, and dendritic arborization of the cells was decreased. The number of myelinated axons, as determined by electron microscopy, was decreased in the mediodorsal portion of the pyramidal tract in the medulla oblongata as well as the specific activity of myelination of the total brain. Thus the functional consequences of vitamin B6 deficits during neuronal development may be through reduced connections among neurons and decreased myelination, which alter the rate and magnitude of transmission of nerve impulses.