ArticlePLoS computational biology2011
Impact of fast sodium channel inactivation on spike threshold dynamics and synaptic integration.
Article in PLoS computational biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 98 citations in OpenAlex.
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- Similarities in the Biophysical Properties of Spiral-Ganglion and Vestibular-Ganglion Neurons in Neonatal Rats.Frontiers in neuroscience · 2021Article
- Simple models including energy and spike constraints reproduce complex activity patterns and metabolic disruptions.PLoS computational biology · 2020Article
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- Spike threshold adaptation diversifies neuronal operating modes in the auditory brain stem.Journal of neurophysiology · 2019Article
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- Loss of Neurofascin-186 Disrupts Alignment of AnkyrinG Relative to Its Binding Partners in the Axon Initial Segment.Frontiers in cellular neuroscience · 2019Article
- Precisely timed inhibition facilitates action potential firing for spatial coding in the auditory brainstem.Nature communications · 2018Article
- Optimal Localist and Distributed Coding of Spatiotemporal Spike Patterns Through STDP and Coincidence Detection.Frontiers in computational neuroscience · 2018Article
- Non-Decaying postsynaptics potentials and delayed spikes in hippocampal pyramidal neurons generated by a zero slope conductance created by the persistent NaChannels (Austin, Tex.) · 2018Article
- Spike threshold dynamics in spinal motoneurons during scratching and swimming.The Journal of physiology · 2017Article
- Calcium-activated SK channels control firing regularity by modulating sodium channel availability in midbrain dopamine neurons.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons spike when their membrane potential exceeds a threshold value. In central neurons, the spike threshold is not constant but depends on the stimulation. Thus, input-output properties of neurons depend both on the effect of presynaptic spikes on the membrane potential and on the dynamics of the spike threshold. Among the possible mechanisms that may modulate the threshold, one strong candidate is Na channel inactivation, because it specifically impacts spike initiation without affecting the membrane potential. We collected voltage-clamp data from the literature and we found, based on a theoretical criterion, that the properties of Na inactivation could indeed cause substantial threshold variability by itself. By analyzing simple neuron models with fast Na inactivation (one channel subtype), we found that the spike threshold is correlated with the mean membrane potential and negatively correlated with the preceding depolarization slope, consistent with experiments. We then analyzed the impact of threshold dynamics on synaptic integration. The difference between the postsynaptic potential (PSP) and the dynamic threshold in response to a presynaptic spike defines an effective PSP. When the neuron is sufficiently depolarized, this effective PSP is briefer than the PSP. This mechanism regulates the temporal window of synaptic integration in an adaptive way. Finally, we discuss the role of other potential mechanisms. Distal spike initiation, channel noise and Na activation dynamics cannot account for the observed negative slope-threshold relationship, while adaptive conductances (e.g. K+) and Na inactivation can. We conclude that Na inactivation is a metabolically efficient mechanism to control the temporal resolution of synaptic integration.
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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.