ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Dynamic regulation of calcium influx by G-proteins, action potential waveform, and neuronal firing frequency.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 102 citations in OpenAlex.
- Kv2 channels contribute to neuronal activity within the vagal afferent-nTS reflex arc.American journal of physiology. Cell physiology · 2024Article
- The computational power of the human brain.Frontiers in cellular neuroscience · 2023Review
- Impaired TRPM3-dependent calcium influx and restoration using Naltrexone in natural killer cells of myalgic encephalomyelitis/chronic fatigue syndrome patients.Journal of translational medicine · 2022Article
- Article
- Modulation of voltage-gated CaChannels (Austin, Tex.) · 2020Review
- The potassium channel subunit KProceedings of the National Academy of Sciences of the United States of America · 2020Article
- TTX-Resistant Sodium Channels Functionally Separate Silent From Polymodal C-nociceptors.Frontiers in cellular neuroscience · 2020Article
- Tetrodotoxin-Sensitive Sodium Channels Mediate Action Potential Firing and Excitability in Menthol-Sensitive Vglut3-Lineage Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Past and Future of Analog-Digital Modulation of Synaptic Transmission.Frontiers in cellular neuroscience · 2019Review
- Modulation of Ion Channels in the Axon: Mechanisms and Function.Frontiers in cellular neuroscience · 2019Review
- Two Forms of Synaptic Depression Produced by Differential Neuromodulation of Presynaptic Calcium Channels.Neuron · 2018Article
- Dopamine-mediated calcium channel regulation in synaptic suppression in L. stagnalis interneurons.Channels (Austin, Tex.) · 2018Article
- Action Potential Broadening in Capsaicin-Sensitive DRG Neurons from Frequency-Dependent Reduction of Kv3 Current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Serotonin and Serotonin Transporters in the Adrenal Medulla: A Potential Hub for Modulation of the Sympathetic Stress Response.ACS chemical neuroscience · 2017Review
- Profound alteration in cutaneous primary afferent activity produced by inflammatory mediators.eLife · 2016Article
- Distinct roles for Cav2.1-2.3 in activity-dependent synaptic dynamics.Journal of neurophysiology · 2014Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Voltage-dependent kappa-opioid modulation of action potential waveform-elicited calcium currents in neurohypophysial terminals.Journal of cellular physiology · 2010Article
- Compensatory regulation of Cav2.1 Ca2+ channels in cerebellar Purkinje neurons lacking parvalbumin and calbindin D-28k.Journal of neurophysiology · 2010Article
- Pathway-specific use-dependent dynamics of excitatory synaptic transmission in rat intracortical circuits.The Journal of physiology · 2007Article
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 1 institution in 1 country.
Funding
Abstract
The time course of Ca2+ channel activation and the amplitude and rate of change of Ca2+ influx are primarily controlled by membrane voltage. G-protein-coupled signaling pathways, however, modulate the efficacy of membrane voltage on channel gating. To study the interactions of membrane potential and G-proteins on Ca2+ influx in a physiological context, we have measured N-type Ca2+ currents evoked by action potential waveforms in voltage-clamped chick dorsal root ganglion neurons. We have quantified the effect of varying action potential waveforms and frequency on the shape of Ca2+ current in the presence and absence of transmitters (GABA or norepinephrine) that inhibit N current. Our results demonstrate that both the profile of Ca2+ entry and the time course and magnitude of its transmitter-induced inhibition are sensitive functions of action potential waveform and frequency. Increases in action potential duration enhance total Ca2+ entry, but they also prolong and blunt Ca2+ signals by slowing influx rate and reducing peak amplitude. Transmitter-mediated inhibition of Ca2+ entry is most robust with short-duration action potentials and decreases exponentially with increasing duration. Increases in action potential frequency promote a voltage-dependent inactivation of Ca2+ influx. In channels exposed to GABA or norepinephrine, however, this inactivation is counteracted by a time- and frequency-dependent relief of modulation. Thus, multiple stimuli are integrated by Ca2+ channels, tuning the profile of influx in a changing physiological environment. Such variations are likely to be significant for the control of Ca2+-dependent cellular responses in all tissues.
Indexed as
Identifiers
9712647PMC6792969W1654673127What OpenQuestion holds
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.