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- W1608214001 abstract "Purpose: Febrile seizures (FS), the most frequent seizure type during childhood, have been linked to temporal lobe epilepsy (TLE) in adulthood. Yet, underlying mechanisms are still largely unknown. Altered γ-aminobutyric acid (GABA)ergic neurotransmission in the dentate gyrus (DG) circuit has been hypothesized to be involved. This study aims at analyzing whether experimental FS change inhibitory synaptic input and postsynaptic GABAAR function in dentate granule cells. Methods: We applied an immature rat model of hyperthermia (HT)–induced FS. GABAAR-mediated neurotransmission was studied using whole-cell patch-clamp recordings from dentate granule neurons in hippocampal slices within 6–9 days post-HT. Key Findings: Frequencies of spontaneous inhibitory postsynaptic currents (sIPSCs) were reduced in HT rats that had experienced seizures, whereas sIPSC amplitudes were enhanced. Whole-cell GABA responses revealed a doubled GABAAR sensitivity in dentate granule cells from HT animals, compared to that of normothermic (NT) controls. Analysis of sIPSCs and whole-cell GABA responses showed similar kinetics in postsynaptic GABAARs of HT and NT rats. quantitative real-time polymerase chain reaction (qPCR) experiments indicated changes in DG GABAAR subunit expression, which was most pronounced for the α3 subunit. Significance: The data support the hypothesis that FS persistently alter neuronal excitability." @default.
- W1608214001 created "2016-06-24" @default.
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- W1608214001 date "2012-10-02" @default.
- W1608214001 modified "2023-10-16" @default.
- W1608214001 title "Experimental early-life febrile seizures induce changes in GABA<sub>A</sub>R-mediated neurotransmission in the dentate gyrus" @default.
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- W1608214001 doi "https://doi.org/10.1111/j.1528-1167.2012.03694.x" @default.
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