ArticleCommunications biology2021
PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Autism-associated SCN2A deficiency disrupts cortico-striatal circuitry in human brain assembloids.Neuron · 2026Article
- Type IIB PKA serves as the primary effector of Gs-coupled receptor-potentiated insulin secretion in mice by orchestrating ion channels and granule phenotype.Diabetologia · 2026Article
- PKA restricts ERK signaling in learning and memory Kenyon cell neurons.Cellular signalling · 2025Article
- Redox Regulation of cAMP-Dependent Protein Kinase and Its Role in Health and Disease.Life (Basel, Switzerland) · 2025Review
- Restoration of excitation/inhibition balance enhances neuronal signal-to-noise ratio and rescues social deficits in autism-associatedbioRxiv : the preprint server for biology · 2025Article
- Review
- Microglial over-pruning of synapses during development in autism-associated SCN2A-deficient mice and human cerebral organoids.Molecular psychiatry · 2024Article
- ADCY3: the pivotal gene in classical ketogenic diet for the treatment of epilepsy.Frontiers in cellular neuroscience · 2024Article
- RIIβ-PKA in GABAergic Neurons of Dorsal Median Hypothalamus Governs White Adipose Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Corticotropin Releasing Factor Mediates KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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Authors and funding
8 authors.
Funding
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Abstract
Temporal lobe epilepsy (TLE) is one of the most common and intractable neurological disorders in adults. Dysfunctional PKA signaling is causally linked to the TLE. However, the mechanism underlying PKA involves in epileptogenesis is still poorly understood. In the present study, we found the autophosphorylation level at serine 114 site (serine 112 site in mice) of PKA-RIIβ subunit was robustly decreased in the epileptic foci obtained from both surgical specimens of TLE patients and seizure model mice. The p-RIIβ level was negatively correlated with the activities of PKA. Notably, by using a P-site mutant that cannot be autophosphorylated and thus results in the released catalytic subunit to exert persistent phosphorylation, an increase in PKA activities through transduction with AAV-RIIβ-S112A in hippocampal DG granule cells decreased mIPSC frequency but not mEPSC, enhanced neuronal intrinsic excitability and seizure susceptibility. In contrast, a reduction of PKA activities by RIIβ knockout led to an increased mIPSC frequency, a reduction in neuronal excitability, and mice less prone to experimental seizure onset. Collectively, our data demonstrated that the autophosphorylation of RIIβ subunit plays a critical role in controlling neuronal and network excitabilities by regulating the activities of PKA, providing a potential therapeutic target for TLE.
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