The neurobiology of antiepileptic drugs
By M. Rogawski, Wolfgang Löscher. Nature Reviews Neuroscience, 2004
1,212 citations recorded by the source corpus.
Antiepileptic drugs (AEDs) provide satisfactory control of seizures for most patients with epilepsy. The drugs have the remarkable ability to protect against seizures while permitting normal functioning of the nervous system. AEDs act on diverse molecular targets to selectively modify the excitability of neurons so that seizure-related firing is blocked without disturbing non-epileptic activity. This occurs largely through effects on voltage-gated sodium and calcium channels, or by promoting inhibition mediated by GABAA (γ-aminobutyric acid, type A) receptors. The subtle biophysical modifications in channel behaviour that are induced by AEDs are often functionally opposite to defects in channel properties that are caused by mutations associated with epilepsy in humans.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/959d768e30d1a777fd954be374a83fb08f17a273
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In Cellular and Molecular Neuroscience
- Maiken Nedergaard
- N. Oberheim
- A. Vezzani
- Heidrun Potschka
- Wolfgang Löscher
- Berislav Zlokovic
- Alexei Verkhratsky
- M. Sofroniew
In Molecular Biology
- Pouya Khankhanian
- Sergio E. Baranzini
- Daniel S. Himmelstein
- Leo Brueggeman
- Wolfgang Löscher
- A. Green
- Maiken Nedergaard
- A. Lizee
In Psychiatry and Mental health
Citations in the corpus
- An astrocytic basis of epilepsy (2005, background): “Epilepsies result from long-lasting plastic changes in the brain affecting the expression of receptors and channels, and involve sprouting and reorganization of synapses, as well as reactive gliosi”
- Drug resistance in brain diseases and the role of drug efflux transporters (2005, neutral): “Despite advances in antiepileptic drug (AED) therap”
- Drug Resistance in Epilepsy: Clinical Impact, Potential Mechanisms, and New Innovative Treatment Options (2020, background): “…for hyperexcitability, may be involved, for example, in reducing target susceptibility to classic ASDs that act on voltage-gated channels (Rogawski and Löscher, 2004) or play a role in SE refractoriness to benzodiazepines and the associated changes in GABAA receptor subunits (Niquet et…”
- The role of inflammation in epilepsy (2010, neutral): “…(for example, suppressor of cytokine signaling proteins) 43 or transcription (for example, Nurr1–CoREST or activity transcription factor 3), 44,45 as well as an array of soluble mediators with anti-inflammatory activities (such as IL-10 and TGF-β ), 46 are produced concomitantly with…”
- Differential distribution of voltage‐gated calcium channel alpha‐2 delta (α2δ) subunit mRNA‐containing cells in the rat central nervous system and the dorsal root ganglia (2005, background): “…to 2 -1 and 2 -2 VGCC subunits is believed to be related to the analgesic effect of gabapentin on neuropathic pain (Gee et al., 1996) and to the antiepileptic effect of gabapentin on epilepsy (Rogawski and Loscher, 2004), but the exact mechanism of action of these effects remains to be determined.”
- Systematic integration of biomedical knowledge prioritizes drugs for repurposing (2017, methodology): “Besides cytochrome P450, which primarily influences pharmacokinetics ( Johannessen and Landmark, 2010 ), our method detected and leveraged bonafide anti-ictogenic mechanisms ( Rogawski and Lo¨scher, 2004 ).”
- The Oscillatory Basis of Working Memory Function and Dysfunction in Epilepsy (2021, background): “AED treatment in epilepsy protects against seizures by modulating neuronal excitability (Rogawski and Löscher, 2004).”