ArticleScientific reports2016
LGI1 acts presynaptically to regulate excitatory synaptic transmission during early postnatal development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 54 citations in OpenAlex.
- A role for leucine-rich, glioma inactivated 1 in regulating pain sensitivity.Brain : a journal of neurology · 2025Article
- LGI1 Autoantibodies Enhance Synaptic Transmission by Presynaptic KNeurology(R) neuroimmunology & neuroinflammation · 2024Article
- Activity-driven synaptic translocation of LGI1 controls excitatory neurotransmission.Cell reports · 2024Article
- Rescue of Normal Excitability in LGI1-Deficient Epileptic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Antibody induced seizure susceptibility and impaired cognitive performance in a passive transfer rat model of autoimmune encephalitis.Frontiers in immunology · 2023Article
- The LGI1 protein: molecular structure, physiological functions and disruption-related seizures.Cellular and molecular life sciences : CMLS · 2021Review
- LGI1 governs neuritin-mediated resilience to chronic stress.Neurobiology of stress · 2021Article
- Epilepsy With Auditory Features: From Etiology to Treatment.Frontiers in neurology · 2021Review
- Structural and Functional Aspects of the Neurodevelopmental GeneFrontiers in molecular neuroscience · 2021Review
- Persistent sodium current blockers can suppress seizures caused by loss of low-threshold D-type potassium currents: Predictions from an in silico study of KEpilepsia open · 2020Article
- Spatially resolved dendritic integration: towards a functional classification of neurons.PeerJ · 2020Article
- Antagonizing IncreasedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Autoimmune seizures and epilepsy.The Journal of clinical investigation · 2019Review
- Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis inInternational journal of molecular sciences · 2019Article
- Quantifying How Staining Methods Bias Measurements of Neuron Morphologies.Frontiers in neuroinformatics · 2019Article
- LGI1 antibodies alter Kv1.1 and AMPA receptors changing synaptic excitability, plasticity and memory.Brain : a journal of neurology · 2018Article
- LGI1 tunes intrinsic excitability by regulating the density of axonal Kv1 channels.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Seizures and Epilepsies due to Channelopathies and Neurotransmitter Receptor Dysfunction: A Parallel between Genetic and Immune Aspects.Molecular syndromology · 2016Review
- Article
- Putting the Horse Before the Cart: Looking to Presynaptic Mechanisms in Genetic Models.Epilepsy currentsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The secreted leucine-rich glioma inactivated 1 (LGI1) protein is an important actor for human seizures of both genetic and autoimmune etiology: mutations in LGI1 cause inherited temporal lobe epilepsy, while LGI1 is involved in antibody-mediated encephalitis. Remarkably, Lgi1-deficient (Lgi1(-/-)) mice recapitulate the epileptic disorder and display early-onset spontaneous seizures. To understand how Lgi1-deficiency leads to seizures during postnatal development, we here investigated the early functional and structural defects occurring before seizure onset in Lgi1(-/-) mice. We found an increased excitatory synaptic transmission in hippocampal slices from Lgi1(-/-) mice. No structural alteration in the morphology of pyramidal cell dendrites and synapses was observed at this stage, indicating that Lgi1-deficiency is unlikely to trigger early developmental abnormalities. Consistent with the presynaptic subcellular localization of the protein, Lgi1-deficiency caused presynaptic defects, with no alteration in postsynaptic AMPA receptor activity in Lgi1-/- pyramidal cells before seizure onset. Presynaptic dysfunction led to increased synaptic glutamate levels, which were associated with hyperexcitable neuronal networks. Altogether, these data show that Lgi1 acts presynaptically as a negative modulator of excitatory synaptic transmission during early postnatal development. We therefore here reveal that increased presynaptic glutamate release is a key early event resulting from Lgi1-deficiency, which likely contributes to epileptogenesis.
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.