Effects of temperature elevation on neuronal inhibition in hippocampal neurons of immature and mature rats

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 study, we investigated the effects of hyperthermia on GABA(A) and GABA(B) receptor-mediated inhibitory postsynaptic currents (IPSCs) in CA1 and DG neurons from immature (11-17 days old) and mature (6-8 weeks old) rats using whole-cell recordings in vitro. In immature rats, hyperthermia decreased the peak amplitude of GABA(A) receptor-mediated IPSCs (GABA(A) IPSCs) in PCs but not in GCs. However, hyperthermia decreased the decay time constant of GABA(A) IPSCs to a similar extent in both PCs and GCs. In mature rats, hyperthermia decreased the peak amplitude but not the decay time constant of GABA(A) IPSCs in both PCs and GCs. Hyperthermia decreased charge transfer (area) of the GABA(A) IPSC of PCs more in immature than in mature rats. In contrast, hyperthermia decreased the GABA(B) receptor-mediated IPSCs to the same degree in immature and mature rats, for either CA1 or DG neurons. Because the hippocampus has been found to be involved in hyperthermia-induced behavioral seizures in immature rats, we suggest that the higher sensitivity of CA1 inhibitory synaptic function to hyperthermia in immature compared with mature rats might partially explain the higher susceptibility for febrile seizures in immature animals.