Maternal dietary tryptophan deficiency alters cardiorespiratory control in rat pups

Abstract

Malnutrition during pregnancy adversely affects postnatal forebrain development; its effect upon brain stem development is less certain. To evaluate the role of tryptophan [critical for serotonin (5-HT) synthesis] on brain stem 5-HT and the development of cardiorespiratory function, we fed dams a diet ∼45% deficient in tryptophan during gestation and early postnatal life and studied cardiorespiratory variables in the developing pups. Deficient pups were of normal weight at postnatal day (P)5 but weighed less than control pups at P15 and P25 (P < 0.001) and had lower body temperatures at P15 (P < 0.001) and P25 (P < 0.05; females only). Oxygen consumption (Vo(2)) was unaffected. At P15, deficient pups had an altered breathing pattern and slower heart rates. At P25, they had significantly lower ventilation (Ve) and Ve-to-Vo(2) ratios in both air and 7% CO(2). The ventilatory response to CO(2) (% increase in Ve/Vo(2)) was significantly increased at P5 (males) and reduced at P15 and P25 (males and females). Deficient pups had 41-56% less medullary 5-HT (P < 0.01) compared with control pups, without a difference in 5-HT neuronal number. These data indicate important interactions between nutrition, brain stem physiology, and age that are potentially relevant to understanding 5-HT deficiency in the sudden infant death syndrome.

Brain stem serotonin protects blood pressure in neonatal rats exposed to episodic anoxia

“…We must consider these sites of 5-HT synthesis and activity when interpreting our findings. Regardless, our data may apply to situations where 5-HT content is reduced globally, including reduced intake of dietary tryptophan (31) or increased alcohol intake (32).…”

Medullary 5-HT neurons: Switch from tonic respiratory drive to chemoreception during postnatal development

“…Their contribution to chemoreception has been characterized in adult mice, but not in neonatal mice. There are a variety of mouse models with dysfunction in their 5-HT system, such as Pet1 −/− mice that have a 70% reduction of 5-HT neurons, Lmx1b f/f/p mice that lack >99% of 5-HT neurons, serotonin transporter (5-HTT) knockout mice that exhibit an absence of 5-HT reuptake and decreased rate of synaptic 5-HT clearance, and others including dietary tryptophan depletion or tryptophan hydroxylase knockout mice (Alenina N et al, 2009; Cummings KJ et al, 2010; Erickson JT et al, 2007; Hodges MR et al, 2009; Holmes A et al, 2003; Li A & Nattie E, 2008; Penatti EM et al, 2011). Some of these mice display respiratory abnormalities, high mortality, and growth retardation in the early postnatal period.…”

A Short-Term Fasting in Neonates Induces Breathing Instability and Epigenetic Modification in the Carotid Body

“…Maternal or prenatal nutrition have been shown to affect ventilatory control systems and could become background etiology of sudden infant death syndrome (Penatti et al 2011). Considering that mild sickness and social economical background are risk factors for SIDS (Spencer and Logan 2004), the current study may have an important clinical implication.…”

“…As to environmental factors, maternal nicotine exposure and inflammation reduce ventilation and increases apnea frequencies (Gauda et al 2013). Recently, an importance of perinatal nutrition for the development of breathing control system has been highlighted (de Brito Alves et al 2014 ; Penatti et al 2011). Maternal deficiency of tryptophan (a precursor for serotonin) during perinatal period alters cardiopulmonary regulation in rat pups.…”