Post natal impact of maternal tryptophan deficiency on central CO2/PH chemosensitivity

Abstract

Serotonergic dysfunction is thought to enhance vulnerability to Sudden Infant Death Syndrome (SIDS) by compromising critical homeostatic reflexes. Rat dams fed a tryptophan deficient diet produce pups with low tissue serotonin (5HT) had a reduced ventilatory sensitivity to inspired CO2 in vivo. We use a perfused in situ brainstem model derived from pups of dams fed either a control or tryptophan deficient diet, to test the hypothesis that developmental tryptophan deficiency alters central CO2/pH chemosensitivity. Pups (P21‐P83) developmentally exposed and maintained on the experimental diet had decreased ventilatory responses to arterial hypercapnia. Results indicate that central chemosensitive mechanisms are influenced by this treatment. We have proposed that raphé 5HT and GABA mediated mechanisms contribute to central CO2/pH chemosensitivity. Current experiments indicate that these mechanisms continue to contribute to the residual chemosensitivity remaining after tryptophan deficiency. These data further illustrate the contributions of 5HT dysfunction to SIDS vulnerability and enhance our understanding of the impacts of pre and postnatal nutrition. Supported by NIH 2U54NS041069‐06A1 (NINDS), and 5P20RR016466 (NCRR).