ArticleBrain : a journal of neurology2022
AMPK-mediated potentiation of GABAergic signalling drives hypoglycaemia-provoked spike-wave seizures.
Article in Brain : a journal of neurology, 2022. 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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12 citing papers in PubMed, 17 citations in OpenAlex.
- Integrative physiology of skeletal muscle for maintaining cognitive health.The Journal of physiology · 2026Review
- The associations between epilepsy, metabolism, and their clinical implications.Frontiers in endocrinology · 2026Review
- Neurochemical and genetic effects of the ketogenic diet: alterations in brain GABA, glutamate, and related gene.Molecular biology reports · 2025Article
- Epilepsy and autophagy modulators: a therapeutic split.Autophagy · 2025Review
- GABAMedComm · 2025Review
- Exploring the clinical connections between epilepsy and diabetes mellitus: Promising therapeutic strategies utilizing agmatine and metformin.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Amino Acid Compound 2 (AAC2) Treatment Counteracts Insulin-Induced Synaptic Gene Expression and Seizure-Related Mortality in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- AMPK role in epilepsy: a promising therapeutic target?Journal of neurology · 2024Review
- New insights on the potential anti-epileptic effect of metformin: Mechanistic pathway.Journal of cellular and molecular medicine · 2023Review
- Autophagy and autophagy signaling in Epilepsy: possible role of autophagy activator.Molecular medicine (Cambridge, Mass.) · 2023Review
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- The role of AMPK-dependent pathways in cellular and molecular mechanisms of metformin: a new perspective for treatment and prevention of diseases.Inflammopharmacology · 2022Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Metabolism regulates neuronal activity and modulates the occurrence of epileptic seizures. Here, using two rodent models of absence epilepsy, we show that hypoglycaemia increases the occurrence of spike-wave seizures. We then show that selectively disrupting glycolysis in the thalamus, a structure implicated in absence epilepsy, is sufficient to increase spike-wave seizures. We propose that activation of thalamic AMP-activated protein kinase, a sensor of cellular energetic stress and potentiator of metabotropic GABAB-receptor function, is a significant driver of hypoglycaemia-induced spike-wave seizures. We show that AMP-activated protein kinase augments postsynaptic GABAB-receptor-mediated currents in thalamocortical neurons and strengthens epileptiform network activity evoked in thalamic brain slices. Selective thalamic AMP-activated protein kinase activation also increases spike-wave seizures. Finally, systemic administration of metformin, an AMP-activated protein kinase agonist and common diabetes treatment, profoundly increased spike-wave seizures. These results advance the decades-old observation that glucose metabolism regulates thalamocortical circuit excitability by demonstrating that AMP-activated protein kinase and GABAB-receptor cooperativity is sufficient to provoke spike-wave seizures.
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