ArticleExperimental brain research2005
Activation of group I metabotropic glutamate receptors depresses recurrent inhibition of motoneurons in the neonatal rat spinal cord in vitro.
Article in Experimental brain research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Developmentally Regulated Modulation of Lumbar Motoneurons by Metabotropic Glutamate Receptors: A Cellular and Behavioral Analysis in Newborn Mice.Frontiers in cellular neuroscience · 2021Article
- Glutamate modulates the firing rate in oculomotor nucleus motoneurons as a function of the recruitment threshold current.The Journal of physiology · 2012Article
- Activation of group I metabotropic glutamate receptors modulates locomotor-related motoneuron output in mice.Journal of neurophysiology · 2011Article
- The effects induced by the sulphonylurea glibenclamide on the neonatal rat spinal cord indicate a novel mechanism to control neuronal excitability and inhibitory neurotransmission.British journal of pharmacology · 2007Article
- Tuning and playing a motor rhythm: how metabotropic glutamate receptors orchestrate generation of motor patterns in the mammalian central nervous system.The Journal of physiology · 2006Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined whether activation of group I metabotropic glutamate receptors (mGluRs) could modulate synaptic inhibition of spinal motoneurons in the neonatal rat isolated spinal cord. Recurrent inhibitory postsynaptic potentials (IPSPs) generated by Renshaw cells were evoked via antidromic stimulation of motor axon collaterals and recorded intracellularly from lumbar motoneurons. The selective agonist of group I mGluRs DHPG (5 micromol L-1) depressed the recurrent IPSP, an effect prevented by the selective antagonist AIDA (500 micromol L-1). The depression by DHPG was use-independent and could be partly counteracted by increasing stimulus strength. Paired pulse depression observed at <or=50-ms intervals was blocked by DHPG in an AIDA-sensitive manner. These results suggest that, in the presence of DHPG, smaller recurrent IPSPs can contribute to the excitatory action of mGluR activation on spinal networks, including the generation of synchronous oscillations recorded from motoneurons.
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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.