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Acute intermittent hypoxia induced neural plasticity in respiratory motor control
Author(s) -
Xing Tao,
Fong Angelina Y,
Bautista Tara G,
Pilowsky Paul M
Publication year - 2013
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12129
Subject(s) - hypoxia (environmental) , intermittent hypoxia , respiratory system , neuroscience , neuroplasticity , biology , control of respiration , synaptic plasticity , facilitation , receptor , medicine , anesthesia , anatomy , chemistry , biochemistry , organic chemistry , oxygen , obstructive sleep apnea
Summary Respiratory neural networks can adapt to rapid environmental change or be altered over the long term by various inputs. The mechanisms that underlie the plasticity necessary for adaptive changes in breathing remain unclear. Acute intermittent hypoxia ( AIH )‐induced respiratory long‐term facilitation ( LTF ) is one of the most extensively studied types of respiratory plasticity. Acute intermittent hypoxia‐induced LTF is present in several respiratory motor outputs, innervating both pump muscles (i.e. diaphragm) and valve muscles (i.e. tongue, pharynx and larynx). Long‐term facilitation is present in various species, including humans, and the expression of LTF is influenced by gender, age and genetics. Serotonin plays a key role in initiating and modulating plasticity at the level of respiratory motor neurons. Recently, multiple intracellular pathways have been elucidated that are capable of giving rise to respiratory LTF . These mainly activate the metabolic receptors coupled to G q (‘Q’ pathway) and G s (‘S’ pathway) proteins. Herein, we discuss AIH ‐induced respiratory LTF in animals and humans, as well as recent advances in our understanding of the synaptic and intracellular pathways underlying this form of plasticity. We also discuss the potential to use intermittent hypoxia to induce functional recovery following cervical spinal injury.