ArticleRespiratory physiology & neurobiology2010
Chronic intermittent hypoxia affects integration of sensory input by neurons in the nucleus tractus solitarii.
Article in Respiratory physiology & neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- In autonomic adaptation the details matter.The Journal of physiology · 2026Article
- Acute intermittent hypoxia enhances nucleus of the solitary tract neuronal activity and requires NMDARs and CaMKII for phrenic long-term facilitation.Journal of neurophysiology · 2025Article
- Reactive Oxidative Species in Carotid Body Chemoreception: Their Role in Oxygen Sensing and Cardiorespiratory Alterations Induced by Chronic Intermittent Hypoxia.Antioxidants (Basel, Switzerland) · 2025Review
- Microglia regulate motor neuron plasticity via reciprocal fractalkine and adenosine signaling.Nature communications · 2024Article
- Oxytocin and corticotropin-releasing hormone exaggerate nucleus tractus solitarii neuronal and synaptic activity following chronic intermittent hypoxia.The Journal of physiology · 2024Article
- Investigating Sea-Level Brain Predictors for Acute Mountain Sickness: A Multimodal MRI Study before and after High-Altitude Exposure.AJNR. American journal of neuroradiology · 2024Article
- Microglia regulate motor neuron plasticity via reciprocal fractalkine/adenosine signaling.bioRxiv : the preprint server for biology · 2024Article
- Article
- Chronic Intermittent Hypoxia reveals role of the Postinspiratory Complex in the mediation of normal swallow production.bioRxiv : the preprint server for biology · 2024Article
- Autonomic Cardiovascular Control in Health and Disease.Comprehensive Physiology · 2023Review
- Nucleus tractus solitarii is required for the development and maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia.Frontiers in physiology · 2023Article
- The role of astrocytes in the nucleus tractus solitarii in maintaining central control of autonomic function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- The protective role of SOD1 overexpression in central mediation of bradycardia following chronic intermittent hypoxia in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Alpha adrenergic receptor signaling in the hypothalamic paraventricular nucleus is diminished by the chronic intermittent hypoxia model of sleep apnea.Experimental neurology · 2021Article
- Apneic Sleep, Insufficient Sleep, and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2019Review
- Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?Frontiers in physiology · 2019Review
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Plasticity in respiratory motor neurons in response to reduced synaptic inputs: A form of homeostatic plasticity in respiratory control?Experimental neurology · 2017Review
- Repetitive acute intermittent hypoxia increases growth/neurotrophic factor expression in non-respiratory motor neurons.Neuroscience · 2016Article
- Age protects from harmful effects produced by chronic intermittent hypoxia.The Journal of physiology · 2016Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The autonomic nervous and respiratory systems, as well as their coupling, adapt over a wide range of conditions. Chronic intermittent hypoxia (CIH) is a model for recurrent apneas and induces alterations in breathing and increases in sympathetic nerve activity which may ultimately result in hypertension if left untreated. These alterations are believed to be due to increases in the carotid body chemoreflex pathway. Here we present evidence that the nucleus tractus solitarii (nTS), the central brainstem termination site of chemoreceptor afferents, expresses a form of synaptic plasticity that increases overall nTS activity following intermittent hypoxia. Following CIH, an increase in presynaptic spontaneous neurotransmitter release occurs under baseline conditions. Furthermore, during and following afferent stimulation there is an augmentation of spontaneous transmitter release that occurs out of synchrony with sensory stimulation. On the other hand, afferent evoked synchronous transmitter release is attenuated. Overall, this shift from synchronous to asynchronous transmitter release enhances nTS cellular discharge. The role of the neurotransmitter dopamine in CIH-induced plasticity is also discussed. Dopamine attenuates synaptic transmission in nTS cells by blockade of N-type calcium channels, and this mechanism occurs tonically following normoxia and CIH. This dopaminergic pathway, however, is not altered in CIH. Taken together, alterations in nTS synaptic activity may play a role in the changes of chemoreflex function and cardiorespiratory activity in the CIH apnea model.
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