The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Enhanced tonic GABAA inhibition in typical absence epilepsy
Open accessAbstract
The cellular mechanisms underlying typical absence seizures, which characterize various idiopathic generalized epilepsies, are not fully understood, but impaired γ-aminobutyric acid (GABA)-ergic inhibition remains an attractive hypothesis. In contrast, we show here that extrasynaptic GABAA receptor–dependent 'tonic' inhibition is increased in thalamocortical neurons from diverse genetic and pharmacological models of absence seizures. Increased tonic inhibition is due to compromised GABA uptake by the GABA transporter GAT-1 in the genetic models tested, and GAT-1 is crucial in governing seizure genesis. Extrasynaptic GABAA receptors are a requirement for seizures in two of the best characterized models of absence epilepsy, and the selective activation of thalamic extrasynaptic GABAA receptors is sufficient to elicit both electrographic and behavioral correlates of seizures in normal rats. These results identify an apparently common cellular pathology in typical absence seizures that may have epileptogenic importance and highlight potential therapeutic targets for the treatment of absence epilepsy.
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Citations
Cites
Variations on an inhibitory theme: phasic and tonic activation of GABAA receptors
Farrant, M., & Nusser, Z. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1625 · Cited by 2,081
Activation of GABAA Receptors: Views from Outside the Synaptic Cleft
Glykys, J., & Mody, I. (2007) · Neuron · doi:10.1016/j.neuron.2007.11.002 · Cited by 358
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Mutations in the GABA Transporter SLC6A1 Cause Epilepsy with Myoclonic-Atonic Seizures
Carvill, G. L., McMahon, J. M., Schneider, A., Zemel, M., Myers, C. T., Saykally, J., Nguyen, J., Robbiano, A., Zara, F., Specchio, N., et al. (2015) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2015.02.016 · Cited by 227
An astroglial basis of major depressive disorder? An overview
Wang, Q., Jie, W., Liu, J., Yang, J., & Gao, T. (2017) · Glia · doi:10.1002/glia.23143 · Cited by 222
Hedrich, U. B. S., Liautard, C., Kirschenbaum, D., Pofahl, M., Lavigne, J., Liu, Y., Theiss, S., Slotta, J., Escayg, A., Dihné, M., et al. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.0721-14.2014 · Cited by 164
Rossignol, E., Kruglikov, I., van den Maagdenberg, A. M. J. M., Rudy, B., & Fishell, G. (2013) · Annals of Neurology · doi:10.1002/ana.23913 · Cited by 112
Metadata
- Authors
- Cope, D. W., Di Giovanni, G., Fyson, S. J., Orbán, G., Errington, A. C., Lőrincz, M. L., Gould, T. M., Carter, D. A., & Crunelli, V.
- Venue
- Nature Medicine
- Published
- 2009-11-22
- Volume
- 15
- Issue
- 12
- Pages
- 1392-1398
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1996957734
- Cited by
- 431
- References
- 3
- FWCI
- 13.66
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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