RESUMO
Vitamin B-6 is an important coenzyme in the biosynthesis of the neurotransmitters GABA, dopamine and serotonin and is therefore required for the normal perinatal development of the central nervous system. In rat studies, biochemical and morphological abnormalities (decreased dendritic arborization and reduced numbers of myelinated axons and synapses) in the brains of pups from vitamin B-6 deficient dams were associated with behavioral changes such as epileptiform seizures and movement disorders. In severely vitamin B-6 deficient human infants, similar behavioral abnormalities have been described. Marginally deficient neonates were found to have a lower birthweight and to display less mature reactive and adaptive behavior in the Brazleton Neonatal Assessment Scale than well-fed infants. While it is not yet possible to define the exact amount of vitamin B-6 required to support optimal brain development, pregnant and lactating women should be encouraged to consume a diet that is rich in vitamin B-6.
Assuntos
Doenças do Sistema Nervoso Central/embriologia , Dopamina/biossíntese , Doenças Neuromusculares/embriologia , Piridoxina/fisiologia , Serotonina/biossíntese , Deficiência de Vitamina B 6/embriologia , Ácido gama-Aminobutírico/biossíntese , Animais , Sistema Nervoso Central/embriologia , Feminino , Humanos , Comportamento do Lactente/fisiologia , Recém-Nascido , Necessidades Nutricionais , Gravidez , Ratos , Fatores de Risco , Espasmos Infantis/embriologiaRESUMO
Effects of maternal restrictions in vitamin B-6 on neuron differentiation and synaptogenesis in developing neocortex were examined. Rats were fed ad libitum a vitamin B-6-free diet supplemented with 0.0 or 0.6 mg pyridoxine hydrochloride (PN.HCl)/kg diet during gestation followed by a control level of 7.0 mg/kg diet during lactation, or they were fed the vitamin B-6-free diet supplemented with 0.6 or 7.0 mg PN.HCl/kg diet throughout gestation and lactation. Neocortices of the offspring were examined at 30 d of age by light and electron microscopy. All maternal restrictions in vitamin B-6 reduced the number of higher order dendrites on stellate neurons in layer II and on pyramidal neurons in layer V of the neocortex and decreased synaptic density in the neuropil of the neocortex. The findings indicated that vitamin B-6 restriction during gestation, either marginal or severe, was the critical treatment factor that adversely affected synaptogenesis and at least one event in neuron differentiation in the neocortex, the arborization of dendrites.
