ArticleScientific reports2019
Deletion of PLCγ1 in GABAergic neurons increases seizure susceptibility in aged mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Urine-Derived iPSC Neurospheres Uncover Proteomic Correlates of Clinical Severity in Dravet Syndrome.Journal of neurochemistry · 2026Article
- Article
- Neural Excitatory/Inhibitory Imbalance in Motor Aging: From Genetic Mechanisms to Therapeutic Challenges.Biology · 2025Review
- Nucleotide metabolism, leukodystrophies, and CNS pathology.Journal of inherited metabolic disease · 2024Review
- PLCγ1 deficiency in chondrocytes accelerates the age-related changes in articular cartilage and subchondral bone.Journal of cellular and molecular medicine · 2024Article
- PLCγ1 in dopamine neurons critically regulates striatal dopamine release via VMAT2 and synapsin III.Experimental & molecular medicine · 2023Article
- Activation Mechanisms and Diverse Functions of Mammalian Phospholipase C.Biomolecules · 2023Review
- Article
- Can Old Animals Reveal New Targets? The Aging and Degenerating Brain as a New Precision Medicine Opportunity for Epilepsy.Frontiers in neurology · 2022Review
- Effects of maternal immune activation in porcine transcript isoforms of neuropeptide and receptor genes.Journal of integrative neuroscience · 2021Article
- The Role of Phospholipase C in GABAergic Inhibition and Its Relevance to Epilepsy.International journal of molecular sciences · 2021Review
- The γ-Protocadherins Regulate the Survival of GABAergic Interneurons during Developmental Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic inhibition plays a fundamental role in the information processing of neural circuits. It sculpts excitatory signals and prevents hyperexcitability of neurons. Owing to these essential functions, dysregulated synaptic inhibition causes a plethora of neurological disorders, including epilepsy, autism, and schizophrenia. Among these disorders, epilepsy is associated with abnormal hyperexcitability of neurons caused by the deficits of GABAergic neuron or decreased GABAergic inhibition at synapses. Although many antiepileptic drugs are intended to improve GABA-mediated inhibition, the molecular mechanisms of synaptic inhibition regulated by GABAergic neurons are not fully understood. Increasing evidence indicates that phospholipase Cγ1 (PLCγ1) is involved in the generation of seizure, while the causal relationship between PLCγ1 and seizure has not been firmly established yet. Here, we show that genetic deletion of PLCγ1 in GABAergic neurons leads to handling-induced seizure in aged mice. In addition, aged Plcg1
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