ArticleEpilepsia open2023
Parvalbumin neurons in the anterior nucleus of thalamus control absence seizures.
Article in Epilepsia open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Deep brain stimulation of the anterior nucleus of the thalamus in animal models of mesial temporal lobe epilepsy: A literature review.Epilepsy research · 2025Review
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
- Absence seizures: Update on signaling mechanisms and networks.Epilepsia open · 2025Article
- Gene therapies alleviate absence epilepsy associated withbioRxiv : the preprint server for biology · 2025Article
- Anticonvulsant effects of pentoxifylline on seizures induced by pentylenetetrazole and maximal electroshock in male mice: The role of the nitrergic pathway.IBRO neuroscience reports · 2024Article
- The Neurovascular Unit Dysfunction in the Molecular Mechanisms of Epileptogenesis and Targeted Therapy.Neuroscience bulletin · 2024Review
- Parvalbumin neurons in the anterior nucleus of thalamus control absence seizures.Epilepsia open · 2023Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAnterior nucleus of thalamus (ANT) has been widely accepted as a potential therapeutic target for drug-resistant epilepsy. Although increased volume of the ANT was also reported in patients with absence epilepsy, the relationship between the ANT and absence epilepsy has been barely illustrated.
methodsUsing chemogenetics, we evaluated the effect of ANT parvalbumin (PV) neurons on pentylenetetrazole (PTZ)-induced absence seizures in mice.
resultsWe found that intraperitoneal injection of PTZ (30 mg/kg) can stably induce absence-like seizures characterized by bilaterally synchronous spike-wave discharges (SWDs). Selective activation of PV neurons in the ANT by chemogenetics could aggravate the severity of absence seizures, whereas selective inhibition of that cannot reverse this condition and even promote absence seizures as well. Moreover, chemogenetic inhibition of ANT PV neurons without administration of PTZ was also sufficient to generate SWDs. Analysis of background EEG showed that chemogenetic activation or inhibition of ANT PV neurons could both significantly increase the EEG power of delta oscillation in the frontal cortex, which might mediate the pro-seizure effect of ANT PV neurons. SIGNIFICANCE: Our findings indicated that either activation or inhibition of ANT PV neurons might disturb the intrinsic delta rhythms in the cortex and worsen absence seizures, which highlighted the importance of maintaining the activity of ANT PV neurons in absence seizure.
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