preprints.org > biology and life sciences > neuroscience and neurology > doi: 10.20944/preprints202307.0702.v1

Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Version 1 : Received: 10 July 2023 / Approved: 11 July 2023 / Online: 11 July 2023 (10:19:23 CEST)

Febrile seizures (FS) are a relatively common early-life condition that can cause CNS developmental disorders, but the specific mechanisms of action of FS are poorly understood. In this work, we used hyperthermia-induced FS in 10-day-old rats. By recording local field potentials, we showed that the efficiency of glutamatergic synaptic transmission decreased 15 min after FS. This effect was transient, and after 2 days there were no differences between control and post-FS groups. During early ontogeny, the proportion of calcium-permeable (CP)-AMPA receptors in the synapses of principal cortical and hippocampal neurons is high. Therefore, rapid internalization of CP-AMPA receptors may be one of the mechanisms underlying this phenomenon. Using the whole-cell patch clamp method and the selective CP-AMPA receptor blocker IEM-1460, we tested whether the proportion of CP-AMPA receptors changes. We have demonstrated that FS rapidly reduces synaptic CP-AMPA receptors in both the hippocampus and the entorhinal cortex. This process was accompanied by a sharp decrease in calcium permeability of the membrane of principal neurons, which we revealed in experiments with kainate-induced cobalt uptake. Our experiments show that FSs cause rapid changes in the function of the glutamatergic system, which may have compensatory effects that prevent excessive excitotoxicity and neuronal death.

febrile seizures; hyperthermia; hippocampus; GluA2-lacking AMPA receptor; entorhinal cortex; IEM-1460; development

Biology and Life Sciences, Neuroscience and Neurology

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