Tsai Min-Lan, Leung L Stan
Program in Neuroscience, University of Western Ontario, London, Ontario, Canada N6A 5C2.
Epilepsia. 2006 Feb;47(2):277-87. doi: 10.1111/j.1528-1167.2006.00419.x.
Whether febrile seizures have detrimental consequences on the brain is still controversial. We hypothesized that neuronal inhibition in the hippocampus is altered after hyperthermia-induced seizures in immature rats.
Rats were given a single seizure by a heat lamp on postnatal day (PND) 15, or repeated seizures by heated air on PND 13 to 15. Fourteen or 30 days after the seizure(s), laminar field potentials were recorded by 16-channel silicon probes in CA1 and the dentate gyrus (DG), in response to the paired-pulse stimulation of the CA3 and medial perforant path, and analyzed as current source density. Gamma-aminobutyric acid (GABA)(B)-receptor antagonist CGP35348 was injected intracerebroventricularly (icv).
At 14 but not at 30 days after a single or after repeated hyperthermia-induced seizures, paired-pulse facilitation (PPF) of the CA1 population spikes at 100 to 200 ms interpulse intervals (IPIs) was significantly increased in seizure as compared with control rats, irrespective of the types of induced seizures. CGP35348 icv also resulted in PPF at 100 to 200 ms IPIs in CA1 of control rats, but CGP35348 had no effect on PPF in seizure rats. At 30 days after repeated seizures, paired-pulse inhibition in the DG was significantly increased at 30-ms IPI, and PPF was increased at 200-ms IPI. CGP35348 increased paired-pulse inhibition in the DG in repeated-seizure rats but not in control rats.
We conclude that hyperthermia-induced seizures in immature rats induced a decrease of GABA(B) receptor-mediated inhibition in CA1 and DG that lasted > or =14 to 30 days after hyperthermic seizure(s).
热性惊厥是否会对大脑产生有害影响仍存在争议。我们推测，未成熟大鼠在热诱导惊厥后海马体中的神经元抑制会发生改变。
在出生后第15天（PND15），用热灯使大鼠发生单次惊厥，或在PND13至15天用热空气使大鼠反复惊厥。在惊厥后14天或30天，用16通道硅探针在CA1和齿状回（DG）记录层流场电位，以响应CA3和内侧穿通通路的双脉冲刺激，并作为电流源密度进行分析。将γ-氨基丁酸（GABA）（B）受体拮抗剂CGP35348脑室内注射（icv）。
在单次或反复热诱导惊厥后14天而非30天，与对照大鼠相比，惊厥大鼠在100至200毫秒脉冲间隔（IPIs）时CA1群体峰电位的双脉冲易化（PPF）显著增加，与诱导惊厥的类型无关。CGP35348脑室内注射也导致对照大鼠CA1在100至200毫秒IPIs时出现PPF，但CGP35348对惊厥大鼠的PPF无影响。在反复惊厥后30天，DG在30毫秒IPI时的双脉冲抑制显著增加，在200毫秒IPI时PPF增加。CGP35348增加了反复惊厥大鼠DG中的双脉冲抑制，但对照大鼠中未增加。
我们得出结论，未成熟大鼠热诱导惊厥导致CA1和DG中GABA（B）受体介导的抑制减少，这种减少在热惊厥后持续≥14至30天。
