ArticleRespiratory physiology & neurobiology2014
Neither serotonin nor adenosine-dependent mechanisms preserve ventilatory capacity in ALS rats.
Article in Respiratory physiology & neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Quantitative assessment of integrated phrenic nerve activity.Respiratory physiology & neurobiology · 2016Pooled it
- SMΝΔ7 mice show breathing and airflow defects with significant pathology of respiratory and oral tract tissues.Frontiers in cellular neuroscience · 2026Article
- The Serotonergic System and Amyotrophic Lateral Sclerosis: A Review of Current Evidence.Cellular and molecular neurobiology · 2023Review
- Tongue and hypoglossal morphology after intralingual cholera toxin B-saporin injection.Muscle & nerve · 2021Article
- Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections.Experimental neurology · 2020Article
- 5-HT2A/B receptor expression in the phrenic motor nucleus in a rat model of ALS (SOD1Respiratory physiology & neurobiology · 2020Article
- Inspiratory pressure-generating capacity is preserved during ventilatory and non-ventilatory behaviours in young dystrophic mdx mice despite profound diaphragm muscle weakness.The Journal of physiology · 2019Article
- Daily acute intermittent hypoxia improves breathing function with acute and chronic spinal injury via distinct mechanisms.Respiratory physiology & neurobiology · 2018Article
- Compensatory plasticity in diaphragm and intercostal muscle utilization in a rat model of ALS.Experimental neurology · 2018Article
- Acute intermittent hypoxia induced phrenic long-term facilitation despite increased SOD1 expression in a rat model of ALS.Experimental neurology · 2015Article
- Stimulation of Respiratory Motor Output and Ventilation in a Murine Model of Pompe Disease by Ampakines.American journal of respiratory cell and molecular biology · 2015Article
- The polymorphic and contradictory aspects of intermittent hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In rats over-expressing SOD1G93A, ventilation is preserved despite significant loss of respiratory motor neurons. Thus, unknown forms of compensatory respiratory plasticity may offset respiratory motor neuron cell death. Although mechanisms of such compensation are unknown, other models of respiratory motor plasticity may provide a conceptual guide. Multiple cellular mechanisms give rise to phrenic motor facilitation; one mechanism requires spinal serotonin receptor and NADPH oxidase activity whereas another requires spinal adenosine receptor activation. Here, we studied whether these mechanisms contribute to compensatory respiratory plasticity in SOD1G93A rats. Using plethysmography, we assessed ventilation in end-stage SOD1G93A rats after: (1) serotonin depletion with parachlorophenylalanine (PCPA), (2) serotonin (methysergide) and A2A (MSX-3) receptor inhibition, (3) NADPH oxidase inhibition (apocynin), and (4) combined treatments. The ability to increase ventilation was not decreased by individual or combined treatments; thus, these mechanisms do not maintain breathing capacity at end-stage motor neuron disease. Possible mechanisms giving rise to enhanced breathing capacity with combined treatment in end-stage SOD1G93A rats are discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.