Diversity of kindling of limbic seizures after lateral fluid percussion injury in the rat

Medel-Matus, Jesús-Servando; Shin, Don; Sankar, Raman; Mazarati, Andréy

doi:10.1002/epi4.12472

Cited by 3 publications

(2 citation statements)

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“…[15][16][17]31 Although admittedly a conjecture until proven directly, such a possibility is supported by our recent finding that a subset of animals subjected to LFPI developed seemingly paradoxical increases of the resistance to kindling of limbic seizures. 23 Together with the report that LPS preconditioning counteracted the acceleration of pentylenetetrazol kindling after controlled cortical impact in rats, 20 makes this scenario a distinct, albeit yet to be proven, prospect.…”

Section: Intestinal Barrier Disruption Vs Endotoxemiamentioning

confidence: 97%

“…Second, as noticed, due to technical challenges, repeated early and late observations were performed in only seven subjects, which limited the interpretation of the time course of the events. Third, low incidence of spontaneous seizures, which is typical for the LFPI model, [21][22][23] made respective statistical analysis even more difficult. Nevertheless, with all the observations considered, several reasonable conclusions can be made.…”

Section: Study Limitationsmentioning

confidence: 99%

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Disruption of intestinal barrier and endotoxemia after traumatic brain injury: Implications for post‐traumatic epilepsy

et al. 2021

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Objective Traumatic brain injury (TBI) may lead to the disruption of the intestinal barrier (IB), and to the escape of products of commensal gut bacteria, including lipopolysaccharide (LPS), into the bloodstream. We examined whether lateral fluid percussion injury (LFPI) and post‐traumatic epilepsy (PTE) are associated with the increased intestinal permeability and endotoxemia, and whether these events in turn are associated with PTE. Methods LFPI was delivered to adult male Sprague‐Dawley rats. Before, 1 week, and 7 months after LFPI, the IB permeability was examined by measuring plasma concentration of fluorescein isothiocyanate–labeled dextran (FD4) upon its enteral administration. Plasma LPS concentration was measured in the same animals, using enzyme‐linked immunosorbent assay. PTE was examined 7 months after LFPI, with use of video‐EEG (electroencephalography) monitoring. Results One week after LFPI, the IB disruption was detected in 14 of 17 and endotoxemia – in 10 of 17 rats, with a strong positive correlation between FD4 and LPS levels, and between plasma levels of each of the analytes and the severity of neuromotor deficit. Seven months after LFPI, IB disruption was detected in 13 of 15 and endotoxemia in 8 of 15 rats, with a strong positive correlation between plasma levels of the two analytes. Five of 15 LFPI rats developed PTE. Plasma levels of both FD4 and LPS were significantly higher in animals with PTE than among the animals without PTE. The analysis of seven rats, which were examined repeatedly at 1 week and at 7 months, confirmed that late IB disruption and endotoxemia were not due to lingering of impairments occurring shortly after LFPI. Significance LFPI leads to early and remote disruption of IB and a secondary endotoxemia. Early and late perturbations may occur in different subjects. Early changes reflect the severity of acute post‐traumatic motor dysfunction, whereas late changes are associated with PTE.

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