Intermittent hypoxia alters the function of cardiovascular neurons and reflex pathways in the brainstem

Document Type

Journal Article

Publication Date



Intermittent Hypoxia and Human Diseases






© Springer-Verlag London 2012. All rights are reserved. Obstructive sleep apnea, and the animal model of this disease, chronic intermittent hypoxia, alters autonomic balance and many different neurobiological functions in the brainstem that likely play an important role in both the initiation and progression of cardiovascular diseases associated with obstructive sleep apnea including hypertension and arrhythmia. Current research suggests the targets of chronic intermittent hypoxia include increased release of the excitatory neurotransmitter glutamate from baroreceptor sensory neurons, likely via altered presynaptic calcium homeostasis and increased spontaneous release of neurotransmitters from these baroreceptor sensory neurons onto brainstem neurons in the nucleus tractus solitarius. Additionally, acute exposures to hypoxia diminish excitatory and enhance inhibitory neurotransmission to parasympathetic cardiac neurons in the nucleus ambiguus that control heart rate and cardiac excitability. Future targets for restoring autonomic balance and increasing survival in these cardiorespiratory diseases require a more thorough understanding of the alterations of synaptic neurotransmission and receptor activation in the brainstem that occur with chronic intermittent hypoxia and obstructive sleep apnea.

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