ArticleNeurobiology of disease2013
Stress, caffeine and ethanol trigger transient neurological dysfunction through shared mechanisms in a mouse calcium channelopathy.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Cerebellar α1Cellular and molecular life sciences : CMLS · 2025Article
- Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei.Dystonia (Lausanne, Switzerland) · 2025Article
- Translating Genetic Discovery into a Mechanistic Understanding of Pediatric Movement Disorders: Lessons from Genetic Dystonias and Related Disorders.Advanced genetics (Hoboken, N.J.) · 2023Article
- What Is the Role of Norepinephrine in Cerebellar Modulation and Stress-Induced Episodic Ataxia?Neurology · 2023Article
- Mechanism of stress-induced attacks in an episodic neurologic disorder.Science advances · 2022Article
- Alcohol alters IL-6 Signal Transduction in the CNS of Transgenic Mice with Increased Astrocyte Expression of IL-6.Cellular and molecular neurobiology · 2021Article
- Aberrant cerebellar Purkinje cell activity as the cause of motor attacks in a mouse model of episodic ataxia type 2.Disease models & mechanisms · 2018Article
- Trauma exposure interacts with the genetic risk of bipolar disorder in alcohol misuse of US soldiers.Acta psychiatrica Scandinavica · 2018Article
- Genetic silencing of olivocerebellar synapses causes dystonia-like behaviour in mice.Nature communications · 2017Article
- Current Opinions and Areas of Consensus on the Role of the Cerebellum in Dystonia.Cerebellum (London, England) · 2017Article
- The PRRT2 knockout mouse recapitulates the neurological diseases associated with PRRT2 mutations.Neurobiology of disease · 2017Article
- The Anatomical Basis for Dystonia: The Motor Network Model.Tremor and other hyperkinetic movements (New York, N.Y.) · 2017Review
- Exercise-induced downbeat nystagmus in a Korean family with a nonsense mutation in CACNA1A.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015Article
- Abnormal excitability and episodic low-frequency oscillations in the cerebral cortex of the tottering mouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Mutational consequences of aberrant ion channels in neurological disorders.The Journal of membrane biology · 2014Review
- The first knockin mouse model of episodic ataxia type 2.Experimental neurology · 2014Article
- Alterations in cerebellar physiology are associated with a stiff-legged gait in Atcay(ji-hes) mice.Neurobiology of disease · 2014Article
- Animal models for dystonia.Movement disorders : official journal of the Movement Disorder Society · 2013Review
- New roles for the cerebellum in health and disease.Frontiers in systems neuroscience · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Several episodic neurological disorders are caused by ion channel gene mutations. In patients, transient neurological dysfunction is often evoked by stress, caffeine and ethanol, but the mechanisms underlying these triggers are unclear because each has diverse and diffuse effects on the CNS. Attacks of motor dysfunction in the Ca(V)2.1 calcium channel mouse mutant tottering are also triggered by stress, caffeine and ethanol. Therefore, we used the tottering mouse attacks to explore the pathomechanisms of the triggers. Despite the diffuse physiological effects of these triggers, ryanodine receptor blockers prevented attacks induced by all of them. In contrast, compounds that potentiate ryanodine receptors triggered attacks suggesting a convergent biochemical pathway. Tottering mouse attacks were both induced and blocked within the cerebellum suggesting that the triggers act locally to instigate attacks. In fact, stress, caffeine and alcohol precipitated attacks in Ca(V)2.1 mutant mice in which genetic pathology was limited to cerebellar Purkinje cells, suggesting that the triggers initiate dysfunction within a specific brain region. The surprising biochemical and anatomical specificity of the triggers and the discovery that the triggers operate through shared mechanisms suggest that it is possible to develop targeted therapies aimed at blocking the induction of episodic neurological dysfunction, rather than treating the symptoms once provoked.
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.