ArticleThe Journal of physiology2002
Molecular determinants of emerging excitability in rat embryonic motoneurons.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Pathophysiology of ion channels in amyotrophic lateral sclerosis.Molecular brain · 2023Review
- Calpain fosters the hyperexcitability of motoneurons after spinal cord injury and leads to spasticity.eLife · 2019Article
- Ion channel dysfunction and altered motoneuron excitability in ALS.Neurological disorders & epilepsy journal · 2019Article
- Ionic Homeostasis Maintenance in ALS: Focus on New Therapeutic Targets.Frontiers in neuroscience · 2018Review
- Complexes of Peptide Blockers with Kv1.6 Pore Domain: Molecular Modeling and Studies with KcsA-Kv1.6 Channel.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- Mutant SOD1 protein increases Nav1.3 channel excitability.Journal of biological physics · 2016Article
- Rbfox proteins regulate alternative splicing of neuronal sodium channel SCN8A.Molecular and cellular neurosciences · 2012Article
- Human induced pluripotent stem cell-derived models to investigate human cytomegalovirus infection in neural cells.PloS one · 2012Article
- Increase of c-Fos and c-Jun expression in spinal and cranial motoneurons of the degenerating muscle mouse (Scn8a(dmu)).Cellular and molecular neurobiology · 2010Article
- Zebrafish motor neuron subtypes differ electrically prior to axonal outgrowth.Journal of neurophysiology · 2009Article
- Neonatal neuronal circuitry shows hyperexcitable disturbance in a mouse model of the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Nodes of Ranvier and axon initial segments are ankyrin G-dependent domains that assemble by distinct mechanisms.The Journal of cell biology · 2007Article
- Early events in node of Ranvier formation during myelination and remyelination in the PNS.Neuron glia biology · 2006Article
- Expression and biophysical properties of Kv1 channels in supragranular neocortical pyramidal neurones.The Journal of physiology · 2006Article
- Differential targeting and functional specialization of sodium channels in cultured cerebellar granule cells.The Journal of physiology · 2005Article
- Where is the spike generator of the cochlear nerve? Voltage-gated sodium channels in the mouse cochlea.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Functional properties of motoneurons derived from mouse embryonic stem cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Some aspects of the physiological role of ion channels in the nervous system.European biophysics journal : EBJ · 2004Review
- Voltage-gated Na+ channel activation induces both action potentials in utricular hair cells and brain-derived neurotrophic factor release in the rat utricle during a restricted period of development.The Journal of physiology · 2003Article
- Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.Channels (Austin, Tex.)Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular determinants of excitability were studied in pure cultures of rat embryonic motoneurons. Using RT-PCR, we have shown here that the spike-generating Na(+) current is supported by Nav1.2 and/or Nav1.3 alpha-subunits. Nav1.1 and Nav1.6 transcripts were also identified. We have demonstrated that alternatively spliced isoforms of Nav1.1 and Nav1.6, resulting in truncated proteins, were predominant during the first week in culture. However, Nav1.6 protein could be detected after 12 days in vitro. The Nav beta 2.1 transcript was not detected, whereas the Nav beta 1.1 transcript was present. Even in the absence of Nav beta 2.1, alpha-subunits were correctly inserted into the initial segment. RT-PCR (at semi-quantitative and single-cell levels) and immunocytochemistry showed that transient K(+) currents result from the expression of Kv4.2 and Kv4.3 subunits. This is the first identification of subunits responsible for a transient K(+) current in spinal motoneurons. The blockage of Kv4.2/Kv4.3 using a specific toxin modified the shape of the action potential demonstrating the involvement of these conductance channels in regulating spike repolarization and the discharge frequency. Among the other Kv alpha-subunits (Kv1.3, 1.4, 1.6, 2.1, 3.1 and 3.3), we showed that the Kv1.6 subunit was partly responsible for the sustained K(+) current. In conclusion, this study has established the first correlation between the molecular nature of voltage-dependent Na(+) and K(+) channels expressed in embryonic rat motoneurons in culture and their electrophysiological characteristics in the period when excitability appears.
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