ArticleJournal of neurophysiology2022
Chronic intermittent hypoxia enhances glycinergic inhibition in nucleus tractus solitarius.
Article in Journal of neurophysiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Chronic intermittent hypoxia increases EPSC frequency in median preoptic nucleus neurons through BDNF-TrkB signaling in a sex-dependent manner.Journal of neurophysiology · 2026Article
- Quantitative and morphological analyses reveal microglia-specific neuroinflammation in brain regions linked to cognitive function in ovariectomized and chronic intermittent hypoxia-exposed female rats.Brain, behavior, & immunity - health · 2026Article
- Chronic intermittent hypoxia drives M1 macrophage polarization in dorsal root ganglia.Brain, behavior, and immunity · 2025Article
- Peripheral macrophages contribute to nociceptor priming in mice with chronic intermittent hypoxia.Science signaling · 2024Article
- Chronic intermittent hypoxia elicits distinct transcriptomic responses among neurons and oligodendrocytes within the brainstem of mice.American journal of physiology. Lung cellular and molecular physiology · 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
- PVN mechanisms in OSA comorbidities: from intermittent hypoxia-stress to therapy.Frontiers in neurologyReview
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic intermittent hypoxia (CIH), an animal model of sleep apnea, has been shown to alter the activity of second-order chemoreceptor neurons in the caudal nucleus of the solitary tract (cNTS). Although numerous studies have focused on excitatory plasticity, few studies have explored CIH-induced plasticity impacting inhibitory inputs to NTS neurons, and the roles of GABAergic and glycinergic inputs on heightened cNTS excitability following CIH are unknown. In addition, changes in astrocyte function may play a role in cNTS plasticity responses to CIH. This study tested the effects of a 7-day CIH protocol on miniature inhibitory postsynaptic currents (mIPSCs) in cNTS neurons receiving chemoreceptor afferents. Normoxia-treated rats primarily displayed GABA mIPSCs, whereas CIH-treated rats exhibited a shift toward combined GABA/glycine-mediated mIPSCs. CIH increased glycinergic mIPSC amplitude and area. This shift was not observed in dorsal motor nucleus of the vagus neurons or cNTS cells from females. Immunohistochemistry showed that strengthened glycinergic mIPSCs were associated with increased glycine receptor protein and were dependent on receptor trafficking in CIH-treated rats. In addition, CIH altered astrocyte morphology in the cNTS, and inactivation of astrocytes following CIH reduced glycine receptor-mediated mIPSC frequency and overall mIPSC amplitude. In cNTS, CIH produced changes in glycine signaling that appear to reflect increased trafficking of glycine receptors to the cell membrane. Increased glycine signaling in cNTS associated with CIH also appears to be dependent on astrocytes. Additional studies will be needed to determine how CIH influences glycine receptor expression and astrocyte function in cNTS.
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