ArticleCNS neuroscience & therapeutics2015
A portion of inhibitory neurons in human temporal lobe epilepsy are functionally upregulated: an endogenous mechanism for seizure termination.
Article in CNS neuroscience & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Transmembrane protein modulates seizure in epilepsy: evidence from temporal lobe epilepsy patients and mouse models.Experimental animals · 2024Article
- Focal seizures are organized by feedback between neural activity and ion concentration changes.eLife · 2022Article
- Cell-specific plasticity associated with integrative memory of triple sensory signals in the barrel cortex.Oncotarget · 2018Article
- Interactions between GHRH and GABAARs in the brains of patients with epilepsy and in animal models of epilepsy.Scientific reports · 2017Article
- PKC and CaMK-II inhibitions coordinately rescue ischemia-induced GABAergic neuron dysfunction.Oncotarget · 2017Article
- Activity-induced spontaneous spikes in GABAergic neurons suppress seizure discharges: an implication of computational modeling.Oncotarget · 2017Article
- Identification of the epileptogenic zone of temporal lobe epilepsy from stereo-electroencephalography signals: A phase transfer entropy and graph theory approach.NeuroImage. Clinical · 2017Article
- Interaction between synaptic inhibition and glial-potassium dynamics leads to diverse seizure transition modes in biophysical models of human focal seizures.Journal of computational neuroscience · 2016Article
- Incoordination among Subcellular Compartments Is Associated with Depression-Like Behavior Induced by Chronic Mild Stress.The international journal of neuropsychopharmacology · 2016Article
- Glucocorticoid Induces Incoordination between Glutamatergic and GABAergic Neurons in the Amygdala.PloS one · 2016Article
- Associations of Unilateral Whisker and Olfactory Signals Induce Synapse Formation and Memory Cell Recruitment in Bilateral Barrel Cortices: Cellular Mechanism for Unilateral Training Toward Bilateral Memory.Frontiers in cellular neuroscience · 2016Article
- Acidosis-Induced Dysfunction of Cortical GABAergic Neurons through Astrocyte-Related Excitotoxicity.PloS one · 2015Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
main problemEpilepsy is one of the more common neurological disorders. The medication is often ineffective to the patients suffering from intractable temporal lobe epilepsy (TLE). As their seizures are usually self-terminated, the elucidation of the mechanism underlying endogenous seizure termination will help to find a new strategy for epilepsy treatment. We aim to examine the role of inhibitory interneurons in endogenous seizure termination in TLE patients.
methodsWhole-cell recordings were conducted on inhibitory interneurons in seizure-onset cortices of intractable TLE patients and the temporal lobe cortices of nonseizure individuals. The intrinsic property of the inhibitory interneurons and the strength of their GABAergic synaptic outputs were measured. The quantitative data were introduced into the computer-simulated neuronal networks to figure out a role of these inhibitory units in the seizure termination.
resultsIn addition to functional downregulation, a portion of inhibitory interneurons in seizure-onset cortices were upregulated in encoding the spikes and controlling their postsynaptic neurons. A patch-like upregulation of inhibitory neurons in the local network facilitated seizure termination. The upregulations of both inhibitory neurons and their output synapses synergistically shortened seizure duration, attenuated seizure strength, and terminated seizure propagation.
conclusionAutomatic seizure termination is likely due to the fact that a portion of the inhibitory neurons and synapses are upregulated in the seizure-onset cortices. This mechanism may create novel therapeutic strategies to treat intractable epilepsy, such as the simultaneous upregulation of cortical inhibitory neurons and their output synapses.
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