In:
Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 14, No. 665 ( 2022-10-05)
Abstract:
Glucose transporter type I deficiency (G1D) is characterized by reduced brain glucose and development of treatment-resistant epilepsy. Here, Rajasekaran et al. use electroencephalography and imaging data from individuals with G1D and showed that the thalamus/sensorimotor cortex circuit might be a critical area involved in the increased brain excitability and the development of seizures. In a mouse model of G1D, the authors showed no energy metabolism impairments, whereas synaptic inhibition of cortical pyramidal and thalamic cells was reduced. Switch in carbon source restored inhibitory activity, and inhibition of AMPA receptor reduced seizures in mice, suggesting that failure of the inhibitory synapses of the circuit might be the main cause of seizure activity in G1D.
Type of Medium:
Online Resource
ISSN:
1946-6234
,
1946-6242
DOI:
10.1126/scitranslmed.abn2956
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
2022
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