ArticleMolecular neurobiology2016
Neuroligin-1 Knockdown Suppresses Seizure Activity by Regulating Neuronal Hyperexcitability.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Transcriptomic analysis reveals differential regulation of synaptic components in pediatric and adult brain tumors.bioRxiv : the preprint server for biology · 2026Article
- Erbin Regulates Neuronal Hyperexcitability and Seizure Susceptibility in Temporal Lobe Epilepsy.Neuroscience bulletin · 2026Article
- The Upregulation of L1CAM by SVHRSP Mitigates Neuron Damage, Spontaneous Seizures, and Cognitive Dysfunction in a Kainic Acid-Induced Rat Model of Epilepsy.Biomolecules · 2025Article
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- Role of Neurexins in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Excitatory synaptic transmission in hippocampal area CA1 is enhanced then reduced as chronic epilepsy progresses.Neurobiology of disease · 2021Article
- Review
- The soluble neurexin-1β ectodomain causes calcium influx and augments dendritic outgrowth and synaptic transmission.Scientific reports · 2020Article
- NL1 expression level in Nrx1β and the excitability of PV interneurons in mice with POCD.Experimental and therapeutic medicine · 2019Article
- Transgenic overexpression of furin increases epileptic susceptibility.Cell death & disease · 2018Article
- ZDHHC8 critically regulates seizure susceptibility in epilepsy.Cell death & disease · 2018Article
- [Erythropoietin accelerates the proliferation of glioma cells via activating Akt pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Pathophysiology of Trans-Synaptic Adhesion Molecules: Implications for Epilepsy.Frontiers in cell and developmental biology · 2018Review
- Inhibition of Calcineurin A by FK506 Suppresses Seizures and Reduces the Expression of GluN2B in Membrane Fraction.Neurochemical research · 2017Article
- Expression of SHANK3 in the Temporal Neocortex of Patients with Intractable Temporal Epilepsy and Epilepsy Rat Models.Cellular and molecular neurobiology · 2017Article
- Synaptic Phospholipid Signaling Modulates Axon Outgrowth via Glutamate-dependent Ca2+-mediated Molecular Pathways.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormally synchronized synaptic transmission in the brain leads to epilepsy. Neuroligin-1 (NL1) is a synaptic cell adhesion molecule localized at excitatory synapses. NL1 modulates synaptic transmission and determines the properties of neuronal networks in the mammalian central nervous system. We showed that the expression of NL1 and its binding partner neurexin-1β was increased in temporal lobe epileptic foci in patients and lithium-pilocarpine-treated epileptic rats. We investigated electrophysiological and behavioral changes in epileptic rats after lentivirally mediated NL1 knockdown in the hippocampus to determine whether NL1 suppression prevented seizures and, if so, to explore the probable underlying mechanisms. Our behavioral studies revealed that NL1 knockdown in epileptic rats reduced seizure severity and increased seizure latency. Whole-cell patch-clamp recordings of CA1 pyramidal neurons in hippocampal slices from NL1 knockdown epileptic rats revealed a decrease in spontaneous action potential frequency and a decrease in miniature excitatory postsynaptic current (mEPSC) frequency but not amplitude. The amplitude of N-methyl-D-aspartate receptor (NMDAR)-dependent EPSCs was also selectively decreased. Notably, NL1 knockdown reduced total NMDAR1 expression and the surface/total ratio in the hippocampus of epileptic rats. Taken together, these data indicate that NL1 knockdown in epileptic rats may reduce the frequency and severity of seizures and suppress neuronal hyperexcitability via changes in postsynaptic NMDARs.
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