ArticleJournal of neurophysiology2013
Slowly inactivating component of Na+ current in peri-somatic region of hippocampal CA1 pyramidal neurons.
Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Persistent sodium currents in neurons: potential mechanisms and pharmacological blockers.Pflugers Archiv : European journal of physiology · 2024Pooled it
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- Effects of GS-967, GS-6615 and ranolazine on the responses of the rabbit aorta to adrenergic nerve stimulation.Frontiers in physiology · 2025Article
- Neuroprotective effect of ranolazine improves behavioral discrepancies in a rat model of scopolamine-induced dementia.Frontiers in neuroscience · 2023Article
- Facilitation of Insulin Effects by Ranolazine in Astrocytes in Primary Culture.International journal of molecular sciences · 2022Article
- Ionic and morphological contributions to the variable gain of membrane responses in layer 2/3 pyramidal neurons of mouse primary visual cortex.Journal of neurophysiology · 2022Article
- Pharmacological intervention in young adolescents rescues synaptic physiology and behavioural deficits in Syngap1Experimental brain research · 2022Article
- Pharmacological determination of the fractional block of Nav channels required to impair neuronal excitability andFrontiers in cellular neuroscience · 2022Article
- Ionic current correlations are ubiquitous across phyla.Scientific reports · 2019Article
- Kinetic properties of persistent NaThe Journal of general physiology · 2018Article
- Persistent Sodium Current Mediates the Steep Voltage Dependence of Spatial Coding in Hippocampal Pyramidal Neurons.Neuron · 2018Article
- Increased transient NaThe Journal of physiology · 2017Article
- Article
- Activation of Ih and TTX-sensitive sodium current at subthreshold voltages during CA1 pyramidal neuron firing.Journal of neurophysiology · 2015Article
- Prototypic and arkypallidal neurons in the dopamine-intact external globus pallidus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- p38 MAP kinase-mediated NMDA receptor-dependent suppression of hippocampal hypersynchronicity in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2014Article
- Effects of SKF83959 on the excitability of hippocampal CA1 pyramidal neurons: a modeling study.Acta pharmacologica Sinica · 2014Article
- Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
The properties of voltage-gated ion channels on the neuronal membrane shape electrical activity such as generation and backpropagation of action potentials, initiation of dendritic spikes, and integration of synaptic inputs. Subthreshold currents mediated by sodium channels are of interest because of their activation near rest, slow inactivation kinetics, and consequent effects on excitability. Modulation of these currents can also perturb physiological responses of a neuron that might underlie pathological states such as epilepsy. Using nucleated patches from the peri-somatic region of hippocampal CA1 neurons, we recorded a slowly inactivating component of the macroscopic Na(+) current (which we have called INaS) that shared many biophysical properties with the persistent Na(+) current, INaP, but showed distinctively faster inactivating kinetics. Ramp voltage commands with a velocity of 400 mV/s were found to elicit this component of Na(+) current reliably. INaS also showed a more hyperpolarized I-V relationship and slower inactivation than those of the fast transient Na(+) current (INaT) recorded in the same patches. The peak amplitude of INaS was proportional to the peak amplitude of INaT but was much smaller in amplitude. Hexanol, riluzole, and ranolazine, known Na(+) channel blockers, were tested to compare their effects on both INaS and INaT. The peak conductance of INaS was preferentially blocked by hexanol and riluzole, but the shift of half-inactivation voltage (V1/2) was only observed in the presence of riluzole. Current-clamp measurements with hexanol suggested that INaS was involved in generation of an action potential and in upregulation of neuronal excitability.
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