ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
The Cav3-Kv4 complex acts as a calcium sensor to maintain inhibitory charge transfer during extracellular calcium fluctuations.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 50 citations in OpenAlex.
- Real-time Monitoring Unveils Three Distinct Neuronal Response Patterns to SAW Ultrasound via L-type Calcium Channels.Neuroscience bulletin · 2026Article
- Cinnarizine, a Calcium Channel Blocker, Partially Prevents the Striatal Dopamine Decline and Loss of Nigral Dopamine Neurons in the Lactacystin-Induced Rat Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- Article
- Calcium-Dependent Regulation of Neuronal Excitability Is Rescued in Fragile X Syndrome by a Tat-Conjugated N-Terminal Fragment of FMRP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- High calcium concentrations reduce cellular excitability of mouse MNTB neurons.Brain research · 2023Article
- Controlling ion channel function with renewable recombinant antibodies.The Journal of physiology · 2022Review
- Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function.International journal of molecular sciences · 2022Review
- Article
- Stellate cell computational modeling predicts signal filtering in the molecular layer circuit of cerebellum.Scientific reports · 2021Article
- Modulation of Kv4.2/KChIP3 interaction by the ceroid lipofuscinosis neuronal 3 protein CLN3.The Journal of biological chemistry · 2020Article
- FMRP(1-297)-tat restores ion channel and synaptic function in a model of Fragile X syndrome.Nature communications · 2020Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
- NCS-1 Deficiency Affects mRNA Levels of Genes Involved in Regulation of ATP Synthesis and Mitochondrial Stress in Highly VulnerableFrontiers in molecular neuroscience · 2019Article
- Diverse Neuron Properties and Complex Network Dynamics in the Cerebellar Cortical Inhibitory Circuit.Frontiers in molecular neuroscience · 2019Article
- Hypothalamic Ion Channels in Hypertension.Current hypertension reports · 2018Review
- Purkinje Cell Signaling Deficits in Animal Models of Ataxia.Frontiers in synaptic neuroscience · 2018Review
- Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors.Channels (Austin, Tex.) · 2018Review
- T-type calcium channels in synaptic plasticity.Channels (Austin, Tex.) · 2017Review
- Long-Term Potentiation at the Mossy Fiber-Granule Cell Relay Invokes Postsynaptic Second-Messenger Regulation of Kv4 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- CACNA1H missense mutations associated with amyotrophic lateral sclerosis alter Cav3.2 T-type calcium channel activity and reticular thalamic neuron firing.Channels (Austin, Tex.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic transmission and neuronal excitability depend on the concentration of extracellular calcium ([Ca](o)), yet repetitive synaptic input is known to decrease [Ca](o) in numerous brain regions. In the cerebellar molecular layer, synaptic input reduces [Ca](o) by up to 0.4 mm in the vicinity of stellate cell interneurons and Purkinje cell dendrites. The mechanisms used to maintain network excitability and Purkinje cell output in the face of this rapid change in calcium gradient have remained an enigma. Here we use single and dual patch recordings in an in vitro slice preparation of Sprague Dawley rats to investigate the effects of physiological decreases in [Ca](o) on the excitability of cerebellar stellate cells and their inhibitory regulation of Purkinje cells. We find that a Ca(v)3-K(v)4 ion channel complex expressed in stellate cells acts as a calcium sensor that responds to a decrease in [Ca]o by dynamically adjusting stellate cell output to maintain inhibitory charge transfer to Purkinje cells. The Ca(v)3-K(v)4 complex thus enables an adaptive regulation of inhibitory input to Purkinje cells during fluctuations in [Ca](o), providing a homeostatic control mechanism to regulate Purkinje cell excitability during repetitive afferent activity.
Indexed as
Identifiers
What 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.