ArticleJournal of neurophysiology2014
Nitric oxide-mediated modulation of the murine locomotor network.
Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Nitric oxide mediates neuro-glial interaction that shapes Drosophila circadian behavior.PLoS genetics · 2020Article
- Pharmacological Characterization of Orofacial Nociception in Female Rats Following Nitroglycerin Administration.Frontiers in pharmacology · 2020Article
- Differential regulation of NMDA receptors by d-serine and glycine in mammalian spinal locomotor networks.Journal of neurophysiology · 2017Article
- Sodium Pumps Mediate Activity-Dependent Changes in Mammalian Motor Networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- A behaviorally related developmental switch in nitrergic modulation of locomotor rhythmogenesis in larval Xenopus tadpoles.Journal of neurophysiology · 2016Article
- Stimulation of Glia Reveals Modulation of Mammalian Spinal Motor Networks by Adenosine.PloS one · 2015Article
- Neuromodulation as a mechanism for the induction of repetition priming.Current opinion in neurobiology · 2014Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Spinal motor control networks are regulated by neuromodulatory systems to allow adaptability of movements. The present study aimed to elucidate the role of nitric oxide (NO) in the modulation of mammalian spinal locomotor networks. This was investigated with isolated spinal cord preparations from neonatal mice in which rhythmic locomotor-related activity was induced pharmacologically. Bath application of the NO donor diethylamine NONOate (DEA/NO) decreased the frequency and modulated the amplitude of locomotor-related activity recorded from ventral roots. Removal of endogenous NO with coapplication of a NO scavenger (PTIO) and a nitric oxide synthase (NOS) blocker [nitro-l-arginine methyl ester (l-NAME)] increased the frequency and decreased the amplitude of locomotor-related activity. This demonstrates that endogenously derived NO can modulate both the timing and intensity of locomotor-related activity. The effects of DEA/NO were mimicked by the cGMP analog 8-bromo-cGMP. In addition, the soluble guanylyl cyclase (sGC) inhibitor ODQ blocked the effects of DEA/NO on burst amplitude and frequency, although the frequency effect was only blocked at low concentrations of DEA/NO. This suggests that NO-mediated modulation involves cGMP-dependent pathways. Sources of NO were studied within the lumbar spinal cord during postnatal development (postnatal days 1-12) with NADPH-diaphorase staining. NOS-positive cells in the ventral horn exhibited a rostrocaudal gradient, with more cells in rostral segments. The number of NOS-positive cells was also found to increase during postnatal development. In summary, we have shown that NO, derived from sources within the mammalian spinal cord, modulates the output of spinal motor networks and is therefore likely to contribute to the fine-tuning of locomotor behavior.
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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.