Consequences of a Maternal Vitamin B6 Deficiency on Hypercapnic Response in Rat Pups

Abstract

Recently, maternal dietary deficiencies have been linked to brainstem neurotransmitter and homeostatic reflex dysfunctions and infant vulnerability to the Sudden Infant Death Syndrome (SIDS). In particular, a gestational and postnatal tryptophan (critical for serotonin, 5HT synthesis) deficiency was shown to induce a serotonergic defect in rat pups, and an attenuated ventilatory response to CO2. We study combined influences of 5HT and the γ‐aminobutyric acid (GABA) mediated chemosensitivity. Vitamin B6 is a coenzyme critical in both 5HT and GABA synthesis. We test the hypothesis that a maternal dietary B6 deficiency (B6d) will alter homeostasis in rat pups. We show multisystem failures with B6d beginning at parturition (P0), reflex disruption when B6d is started at P5, and little effect of B6d started at P10. Data suggest a critical period for B6d sensitivity and the potential that B6d‐induced 5HT and GABAergic deficiencies to produce homeostatic dysfunction that could also influence vulnerability to SIDS. Supported by NIH 2U54NS041069–06A1 and 5P20RR016466.