RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during CNS viral infection DOI Creative Commons
Irving Estevez,

Benjamin D. Buckley,

Nicholas Panzera

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: April 28, 2024

Summary While recent work has identified roles for immune mediators in the regulation of neural activity, capacity cell intrinsic innate signaling within neurons to influence neurotransmission remains poorly understood. However, existing evidence linking with neuronal function suggests that modulation may serve previously undefined host protection during infection central nervous system. Here, we identify a specialized RIPK3, kinase traditionally associated necroptotic death, preserving survival neurotropic flavivirus through suppression excitatory neurotransmission. We show RIPK3 coordinates transcriptomic changes suppress glutamate signaling, thereby desensitizing excitotoxic death. These effects occur independently traditional functions promoting necroptosis and inflammatory transcription. Instead, promotes phosphorylation key regulatory CaMKII, which turn activates transcription factor CREB drive neuroprotective transcriptional program deleterious glutamatergic signaling. findings an unexpected canonical death protein viral highlighting new mechanisms neuroimmune crosstalk.

Language: Английский

The kinase RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during central nervous system viral infection DOI
Irving Estevez,

Benjamin D. Buckley,

Marissa Lindman

et al.

Immunity, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

1
Sleep links hippocampal propensity for epileptiform activity to its viscerosensory inputs DOI Creative Commons
Ekaterina Levichkina, David B. Grayden, Steven Petrou

et al.

Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: March 13, 2025

The development of a seizure relies on two factors. One is the existence an overexcitable neuronal network and other trigger that switches normal activity into paroxysmal state. While mechanisms local overexcitation have been focus many studies, process triggering remains poorly understood. We suggest that, apart from known exteroceptive sources reflex epilepsy such as visual, auditory or olfactory signals, there range interoceptive triggers, which are relevant for in Temporal Lobe Epilepsy (TLE). hypothesis proposed here aims to explain prevalence epileptic sleep drowsiness states provide detailed mechanism seizures triggered by signals.

Language: Английский

Citations

0
Comparative Efficacy of Neuromodulatory Strategies for Drug-Resistant Epilepsy: A Systematic Review and Meta-Analysis DOI Creative Commons
Jianwei Shi,

Dafeng Lu,

Penghu Wei

et al.

World Neurosurgery, Journal Year: 2024, Volume and Issue: 193, P. 373 - 396

Published: Oct. 16, 2024

The study aims to evaluate the efficacy of neuromodulatory strategies for people who have drug-resistant epilepsy (DRE). We searched electronic repositories, including PubMed, Web Science, Embase, and Cochrane Library, randomized controlled trials, their ensuing open-label extension studies, prospective studies focusing on surgical or neuromodulation interventions with DRE. used seizure frequency reduction as primary outcome. A single-arm meta-analysis synthesized data across all assess treatment effectiveness at multiple time points. network evaluated diverse therapies in trials. Grading Recommendations, Assessment, Development, Evaluations was applied overall quality evidence. Twenty-eight representing 2936 individuals underwent 10 treatments were included. Based cumulative ranking meta-analysis, top 3 options deep brain stimulation (DBS) 27% probability, responsive neurostimulation (RNS) 22.91%, transcranial direct current 24.31%. In short-to-medium term, control is more effective RNS than invasive vagus nerve (inVNS), which turn slightly DBS, though differences are minimal. However, long inVNS appears be less both DBS RNS. Trigeminal stimulation, magnetic alternating did not demonstrate significant reduction. Regarding long-term efficacy, outperformed inVNS. While transcutaneous auricular VNS showed promise treating DRE, further needed confirm efficacy.

Language: Английский

Citations

3
Deep brain stimulation DOI
Joachim K. Krauss, Johanna Nagel

Elsevier eBooks, Journal Year: 2024, Volume and Issue: unknown, P. 16 - 41

Published: Aug. 7, 2024

Language: Английский

Citations

2
Therapeutic approaches targeting seizure networks DOI Creative Commons

Jenna Langbein,

Ujwal Boddeti,

Matthew Kreinbrink

et al.

Frontiers in Network Physiology, Journal Year: 2024, Volume and Issue: 4

Published: Aug. 7, 2024

Epilepsy is one of the most common neurological disorders, affecting over 65 million people worldwide. Despite medical management with anti-seizure medications (ASMs), many patients fail to achieve seizure freedom, one-third having drug-resistant epilepsy (DRE). Even surgical through resective surgery and/or neuromodulatory interventions, 50

Language: Английский

Citations

2
RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during CNS viral infection DOI Creative Commons
Irving Estevez,

Benjamin D. Buckley,

Nicholas Panzera

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: April 28, 2024

Summary While recent work has identified roles for immune mediators in the regulation of neural activity, capacity cell intrinsic innate signaling within neurons to influence neurotransmission remains poorly understood. However, existing evidence linking with neuronal function suggests that modulation may serve previously undefined host protection during infection central nervous system. Here, we identify a specialized RIPK3, kinase traditionally associated necroptotic death, preserving survival neurotropic flavivirus through suppression excitatory neurotransmission. We show RIPK3 coordinates transcriptomic changes suppress glutamate signaling, thereby desensitizing excitotoxic death. These effects occur independently traditional functions promoting necroptosis and inflammatory transcription. Instead, promotes phosphorylation key regulatory CaMKII, which turn activates transcription factor CREB drive neuroprotective transcriptional program deleterious glutamatergic signaling. findings an unexpected canonical death protein viral highlighting new mechanisms neuroimmune crosstalk.

Language: Английский

Citations

1