2009
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Abstract: Febrile seizures are the most common seizure type in children, and hyperthermia may contribute to seizure generation during fever. We have previously demonstrated that hyperthermia suppressed gamma-aminobutyric acid (GABA)-ergic synaptic transmission in CA1 neurons of immature rats. However, whether this suppression is age-dependent is unknown. Moreover, it is unclear whether hyperthermia has differential effects on neuronal inhibition in CA1 pyramidal cells (PCs) and dentate gyrus granule cells (GCs). In this… Show more

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“…Temperatures in the range of fever increase synchronization in hippocampal slices, leading to epileptic activity (Tancredi et al 1992;Wu et al 2001). A decrease in GABAergic transmission has also been described as a consequence of hyperthermia (38.5-40°C) (Qu and Leung 2009), particularly in immature rats. We describe here that the activity during up states becomes more synchronized, in the sense that up states have a steep down to up transition and high firing rates are concentrated in short up states, but epileptiform discharges were not observed.…”
Section: Discussionmentioning
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“…Temperatures in the range of fever increase synchronization in hippocampal slices, leading to epileptic activity (Tancredi et al 1992;Wu et al 2001). A decrease in GABAergic transmission has also been described as a consequence of hyperthermia (38.5-40°C) (Qu and Leung 2009), particularly in immature rats. We describe here that the activity during up states becomes more synchronized, in the sense that up states have a steep down to up transition and high firing rates are concentrated in short up states, but epileptiform discharges were not observed.…”
Section: Discussionmentioning
“…In clinics, a high temperature has frequently been reported to trigger seizures. Because GABA A inhibitory synaptic transmission is highly sensitive to temperature, decreasing the temperature serves as a convulsant drug [44]. …”
Section: Discussionmentioning
“…Therefore, this finding raises the possibility that the observed decrease in fast interneuron synchronous discharges on cooling might contribute to the antiepileptic activity of cooling by disturbing the normal synchrony between different cell types and networks in the hippocampus, hence aborting epileptiform discharges within in vitro models of ictogenesis. Furthermore, the persistence of action potential firing in interneurons would have an additional antiepileptic effect through tonic GABA release, and cooling will induce prolongation of decay of phasic inhibitory synaptic current, similar to the effect of benzodiazepines and barbiturates [28].…”
Section: Discussionmentioning
“…The decay, and to a lesser extent, the amplitude of GABA A -mediated inhibitory synaptic currents are very sensitive to temperature changes. Indeed, hyperthermia by decreasing charge transfer at the synapse acts as a convulsant agent [28]. Although the exact ictogenic mechanism in childhood febrile seizures is unclear, it has been associated with temperature-dependent changes in synaptic efficacy consequent to mutations involving the GABA A γ2 subunit [29,30].…”
Section: Discussionmentioning