Liebregts Michelle T, McLachlan Richard S, Leung L Stan
Graduate Program in Neuroscience, University of Western Ontario, London, Ontario, Canada.
Ann Neurol. 2002 Sep;52(3):318-26. doi: 10.1002/ana.10285.
The mechanisms underlying the generation of febrile seizures are poorly understood. This study investigated hyperthermia-induced changes in the hippocampus, a structure implicated in febrile seizures. It was hypothesized that neuronal excitability in the hippocampus changes with increasing temperature, and that this change is different in adult as compared with immature rats. Adult and immature (15-17 days postnatal) male rats were studied under urethane anesthesia during normothermia, moderate hyperthermia (38-39.5 degrees C), and severe hyperthermia (>39.5 degrees C). Paired-pulse inhibition of the orthodromically activated population spikes in the dentate gyrus and cornu ammonis 1 region of the hippocampus (CA1), two structures within the hippocampus, was measured after stimulation of the medial perforant path and Schaffer collaterals, respectively. In the adult rat, paired-pulse inhibition was increased in the dentate gyrus during moderate and severe hyperthermia but decreased in CA1 during severe hyperthermia (all p values < 0.05). In the immature rat, paired-pulse inhibition was unchanged in the dentate gyrus but decreased in CA1 during moderate hyperthermia (p < 0.05). We suggest that hyperthermia contributes to seizure susceptibility in the immature hippocampus by decreasing CA1 inhibition. In the adult rat, a decrease in CA1 inhibition requires a higher degree of hyperthermia, and hippocampal seizure generation is opposed by an increase in dentate gyrus inhibition.
热性惊厥产生的潜在机制尚不清楚。本研究调查了高温诱导的海马体变化，海马体是一个与热性惊厥有关的结构。研究假设，海马体中的神经元兴奋性会随着温度升高而变化，并且与未成熟大鼠相比，成年大鼠的这种变化有所不同。在体温正常、中度高温（38 - 39.5摄氏度）和重度高温（>39.5摄氏度）条件下，对成年和未成熟（出生后15 - 17天）雄性大鼠进行乌拉坦麻醉后进行研究。分别刺激内侧穿通通路和海马体的Schaffer侧支后，测量海马体齿状回和海马体1区（CA1）中正向激活的群体峰电位的双脉冲抑制，齿状回和CA1是海马体内的两个结构。在成年大鼠中，中度和重度高温期间齿状回的双脉冲抑制增加，但重度高温期间CA1的双脉冲抑制降低（所有p值<0.05）。在未成熟大鼠中，齿状回的双脉冲抑制没有变化，但中度高温期间CA1的双脉冲抑制降低（p<0.05）。我们认为，高温通过降低CA1抑制作用，导致未成熟海马体的癫痫易感性增加。在成年大鼠中，CA1抑制作用的降低需要更高程度的高温，并且齿状回抑制作用的增加会对抗海马体癫痫的产生。
