Journal
EPILEPSY & BEHAVIOR
Volume 14, Issue 4, Pages 577-581Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yebeh.2009.01.019
Keywords
Atypical absence seizures; GABA(B)R1b receptors; Slow spike-and-wave discharges; Long-term potentiation; Behavior
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Funding
- Canadian Institutes of Health Research
- Bloorview Children's Hospital Foundation
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Overexpression of GABA(B)R1a receptors in mice (R1a(+)) results in an atypical absence seizure phenotype characterized by 3- to 6-Hz slow spike-and-wave discharges (SSWDs), reduced synaptic plasticity, and cognitive impairment. Here we tested the hypothesis that increased R1 expression causes atypical absence epilepsy and is not subunit specific. GABA(B)R1b receptors were overexpressed in mouse forebrain (R1b(+)) and confirmed by immunoblot and H-3-CGP54626A autoradiography. The R1b(+) mice showed a reduction in hippocampal long-term potentiation and GABA(A) receptor-mediated inhibitory postsynaptic currents. R1b(+) mice manifested an electrographic, pharmacological, and behavioral phenotype consistent with atypical absence seizures, though less robust than R1a(+) in terms of SSWD duration and severity of cognitive impairment. These results suggest that abnormal GABA(B)R1b function plays a lesser role in the development of atypical absence epilepsy. (C) 2009 Elsevier Inc. All rights reserved.
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