Russian Journal of PhysiologyRussian Journal of PhysiologyРоссийский физиологический журнал им. И.М. Сеченова0869-81392658-655XThe Russian Academy of Sciences68089710.31857/S0869813925040029UFKCTLEXPERIMENTAL ARTICLESЭКСПЕРИМЕНТАЛЬНЫЕ СТАТЬИResearch ArticleThe Impact of Febrile Seizures on Synaptic Transmission in the Hippocampus of Rats with Freezing-Induced Focal Cortical DysplasiaВлияние фебрильных судорог на синаптическую передачу в гиппокампе крыс с фокальной кортикальной дисплазией, вызванной замораживаниемPostnikovaT. Y.ПостниковаТ. Ю.
Russian Federation
tapost2@mail.ruZaitsevA. V.ЗайцевА. В.
Russian Federation
tapost2@mail.ruSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of SciencesИнститут эволюционной физиологии и биохимии им. И.М. Сеченова РАН15042025111458159328052025Copyright ©; 2025, Russian Academy of SciencesCopyright ©; 2025, Российская академия наук2025Russian Academy of SciencesРоссийская академия наукhttps://journals.eco-vector.com/0869-8139/article/view/680897

Febrile seizures (FS) in early childhood can lead to the development of epilepsy; however, in most cases, they resolve without consequences. The neurophysiological mechanisms that protect the brain from the effects of FS remain poorly understood. It is also known that the risk of epilepsy significantly increases if a child has congenital abnormalities in the structure of the cerebral cortex. In this study, we examined functional changes in the hippocampus of young rats subjected to FS on the 10th postnatal day (P10) with freezing-induced focal cortical dysplasia (FCD) on P0. Experiments were conducted on three groups of animals: 1) control group (Ctrl) – rats without FS and FCD; 2) FS group – rats subjected to hyperthermia-induced FS on P10; 3) FS+FCD group – rats with cortical freezing on P0 and FS on P10. Using recordings of local synaptic potentials in the CA1 region of the hippocampus, we found that FS led to significant changes in synaptic transmission. In the FS group, there was an increase in the threshold for population spike generation, a decrease in the synaptic transmission efficacy ratio, and an increase in the paired-pulse ratio. These changes indicate reduced activity of CA3-CA1 glutamatergic synapses, which may represent a compensatory response preventing epileptogenesis. However, in the FS+FCD group, such compensatory changes were absent: synaptic transmission parameters did not differ from those in the control group. This suggests that FCD impedes the activation of protective mechanisms in the hippocampus in response to FS. Thus, the presence of cortical dysplasia may increase the risk of epilepsy following FS by 20 blocking natural compensatory processes. Our results highlight the importance of studying the interaction between congenital cortical developmental abnormalities and the consequences of FS for understanding the mechanisms of epileptogenesis.

Фебрильные судороги (ФС) в раннем возрасте могут приводить к развитию эпилепсии, однако в большинстве случаев они проходят бесследно. При этом нейрофизиологические механизмы, защищающие мозг от последствий ФС, остаются малоизученными. Также известно, что риск развития эпилепсии значительно повышается, если у ребенка есть врожденные аномалии в строении коры головного мозга. В данном исследовании мы изучили функциональные изменения в гиппокампе молодых крыс, подвергшихся ФС на 10-й постнатальный день (P10), с фокальной кортикальной дисплазией (ФКД), вызванной замораживанием коры на P0. Эксперименты проводились на трех группах животных: 1) контрольная группа (Ctrl) – крысы без ФС и ФКД; 2) группа с ФС (FS) – крысы, подвергшиеся гипертермии с развитием ФС на P10; 3) группа с ФС и ФКД (FS+FCD) – крысы с замораживанием коры на P0 и ФС на P10. Используя регистрацию локальных синаптических потенциалов в области CA1 гиппокампа, мы выявили, что ФС привели к значительным изменениям в синаптической передаче. В группе FS наблюдалось повышение порога генерации популяционного спайка, снижение коэффициента эффективности синаптической передачи и увеличение коэффициента парной стимуляции. Эти изменения указывают на снижение активности глутаматергических синапсов CA3-CA1, что может быть компенсаторной реакцией, предотвращающей эпилептогенез. Однако в группе FS+FCD такие компенсаторные изменения отсутствовали: показатели синаптической передачи не отличались от контрольной группы. Это свидетельствует о том, что ФКД препятствует запуску защитных механизмов в гиппокампе в ответ на ФС. Таким образом, наличие кортикальной дисплазии может повышать риск развития эпилепсии после ФС, блокируя естественные компенсаторные процессы. Наши результаты подчеркивают важность изучения взаимодействия между врожденными аномалиями развития коры и последствиями ФС для понимания механизмов эпилептогенеза.

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