Invited Review: Neural network plasticity in respiratory control

2003 ◽  
Vol 94 (3) ◽  
pp. 1242-1252 ◽  
Author(s):  
K. F. Morris ◽  
D. M. Baekey ◽  
S. C. Nuding ◽  
T. E. Dick ◽  
R. Shannon ◽  
...  
Keyword(s):  
Brain Stem ◽  
Motor Pattern ◽  
Sleep Apnea Syndrome ◽  
Respiratory Rhythm ◽  
Respiratory Control ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Cord Injury ◽  
Network Plasticity

Respiratory network plasticity is a modification in respiratory control that persists longer than the stimuli that evoke it or that changes the behavior produced by the network. Different durations and patterns of hypoxia can induce different types of respiratory memories. Lateral pontine neurons are required for decreases in respiratory frequency that follow brief hypoxia. Changes in synchrony and firing rates of ventrolateral and midline medullary neurons may contribute to the long-term facilitation of breathing after brief intermittent hypoxia. Long-term changes in central respiratory motor control may occur after spinal cord injury, and the brain stem network implicated in the production of the respiratory rhythm could be reconfigured to produce the cough motor pattern. Preliminary analysis suggests that elements of brain stem respiratory neural networks respond differently to hypoxia and hypercapnia and interact with areas involved in cardiovascular control. Plasticity or alterations in these networks may contribute to the chronic upregulation of sympathetic nerve activity and hypertension in sleep apnea syndrome and may also be involved in sudden infant death syndrome.

Some aspects of clinical relevance in the maturation of respiratory control in infants

2008 ◽  
Vol 104 (6) ◽  
pp. 1828-1834 ◽  
Author(s):  
Bradley T. Thach
Keyword(s):  
Brain Stem ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Clinical Relevance ◽  
Respiratory Control ◽  
Sudden Infant Death ◽  
Pulmonary Aspiration ◽  
Severe Hypoxia ◽  
Sudden Infant ◽  
Major Function

Two reflex mechanisms important for survival are discussed. Brain stem and cardiovascular mechanisms that are responsible for recovery from severe hypoxia (autoresuscitation) are important for survival in acutely hypoxic infants and adults. Failure of this mechanism may be important in sudden infant death syndrome (SIDS), because brain stem-mediated hypoxic gasping is essential for successful autoresuscitation and because SIDS infants appear to attempt to autoresuscitate just before death. A major function of another mechanism is to protect the airway from fluid aspiration. The various components of the laryngeal chemoreflex (LCR) change during maturation. The LCR is an important cause of prolonged apneic spells in infants. Consequently, it also may have a role in causing SIDS. Maturational changes and/or inadequacy of this reflex may be responsible for pulmonary aspiration and infectious pneumonia in both children and adults.

The Uvula and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 319-320
Author(s):  
CHRISTIAN GUILLEMINAULT
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sleep Apnea Syndrome ◽  
Sudden Infant Death ◽  
Term Infant ◽  
Near Miss ◽  
Sudden Infant ◽  
Obstructive Sleep

In Reply.— Harpey and Renault postulate a relationship between the uvula, obstructive sleep apnea, and sudden infant death syndrome. Although I believe that obstructive sleep apnea syndrome may be one of the mechanisms leading to sudden infant death syndrome, this speculation is extremely controversial. I do concur with Harpey and Renault that obstructive sleep apnea can trigger esophageal reflux. A segment from a sleep recording of a 9-week-old, full-term infant with near-miss sudden infant death syndrome is presented in the Figure.

Incidence of Apnea in Siblings of Sudden Infant Death Syndrome Victims Studied at Home

PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 128-131
Author(s):  
Dorothy H. Kelly ◽  
Joseph Twanmoh ◽  
Daniel C. Shannon
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Chronic Hypoxia ◽  
Breathing Pattern ◽  
Respiratory Control ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Sibling Group

Victims of sudden infant death syndrome (SIDS) have been shown to have pathologic abnormalities consistent with chronic hypoxia.1-7 Two groups of infants at high risk of dying of SIDS, near miss infants and subsequent siblings of SIDS victims, have been studied in attempts to demonstrate physiologic abnormalities that could account for these pathologic findings. Investigators have found abnormalities in breathing pattern and the respiratory control system in the former consisting of prolonged sleep apnea, excessive short apnea, periodic breathing, hypoventilation, and depressed response to hypercarbia.8-13 However, studies in the SIDS sibling group have demonstrated varying results of excessive periodic breathing in the home14 and decreased apnea in the laboratory.15

Polymorphisms in genes of respiratory control and sudden infant death syndrome

2015 ◽  
Vol 129 (5) ◽  
pp. 977-984 ◽  
Author(s):  
Katharina Läer ◽  
Thilo Dörk ◽  
Marielle Vennemann ◽  
Thomas Rothämel ◽  
Michael Klintschar
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Respiratory Control ◽  
Sudden Infant Death ◽  
Sudden Infant

scholarly journals Maternal dietary tryptophan deficiency alters cardiorespiratory control in rat pups

2011 ◽  
Vol 110 (2) ◽  
pp. 318-328 ◽  
Author(s):  
Eliana M. Penatti ◽  
Alexis E. Barina ◽  
Sharat Raju ◽  
Aihua Li ◽  
Hannah C. Kinney ◽  
...  
Keyword(s):  
Brain Stem ◽  
Sudden Infant Death ◽  
Normal Weight ◽  
Sudden Infant ◽  
Postnatal Life ◽  
Cardiorespiratory Control ◽  
Cardiorespiratory Function ◽  
Rat Pups ◽  
Neuronal Number

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 (V̇o2) was unaffected. At P15, deficient pups had an altered breathing pattern and slower heart rates. At P25, they had significantly lower ventilation (V̇e) and V̇e-to-V̇o2 ratios in both air and 7% CO2. The ventilatory response to CO2 (% increase in V̇e/V̇o2) 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.

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