Plasticity and metaplasticity of lateral perforant path in hippocampal dentate gyrus in a rat model of febrile seizure / 生理学报

ABSTRACT

Febrile seizure (FS) is common in childhood and can impair cognitive function. The potential to exhibit plasticity at many synapses appears to be modulated by prior synaptic activity. This intriguing higher-order form of plasticity has been termed metaplasticity. Plasticity and metaplasticity have been considered to be one of the most important neurological fundaments of learning and memory. In the present study, field potential recording was carried out to detect the effects of FS on plasticity and metaplasticity in the lateral perforant path of rat hippocampus. Brain slices from rat pups of FS model were prepared and superfused. The recording electrodes were placed within the outer molecular layer for recording of lateral perforant path field excitatory postsynaptic potentials (fEPSP). Stimulation of the lateral perforant path and the dentate hilar region was carried out by placing bipolar stimulating electrodes within the outer molecular layer and hilus, respectively. The results showed that long term potentiation (LTP) of control and FS rats didn't show significant difference after 100 Hz conditioning stimulation. Subjected to 10 Hz priming stimulation applied to lateral perforant path or dentate hilar region 40 min prior to 100 Hz conditioning, the LTP of control group was inhibited, while the LTP of FS rats remained constant. Normalized fEPSP slope 1 h after tetanization of control group was 1.10 ± 0.26 and 1.15 ± 0.14 after homosynaptic and antidromic priming stimulation respectively. On the contrast, FS group didn't show any depression of LTP after homosynaptic and antidromic priming stimulation, normalized fEPSP slope 1 h after tetanization being 1.35 ± 0.2 and 1.47 ± 0.19, respectively. These results suggest that FS would impair lateral perforant path metaplasticity without affecting LTP. These findings represent an intriguing phenomenon of FS-caused brain damage and imply the injury of excitatory status in different pathways.