Volumetric response of the adult brain to seizures depends on the developmental stage when systemic inflammation was induced.

Inflammation has detrimental influences on the developing brain including triggering the epileptogenesis. On the other hand, seizure episodes may induce inflammatory processes and further increase of brain excitability. The present study focuses on the problem whether transitory systemic inflammation during developmental period may have critical importance to functional and/or structural features of the adult brain.

Inflammation in the developing rat modulates astroglial reactivity to seizures in the mature brain.

Astrocytes participate in neuronal development and excitability, and produce factors enhancing or suppressing inflammatory processes occurring due to neurodegenerative diseases, such as epilepsy. Seizures, in turn, trigger the release of inflammatory mediators, causing structural and functional changes in the brain. Therefore, it appears reasonable to determine whether generalized inflammation at developmental periods can affect astrocyte reactivity to epileptic seizures occurring in the adult brain.

Physical training decreases susceptibility to pilocarpine-induced seizures in the injured rat brain.

There is growing evidence that physical activity ameliorates the course of epilepsy in animal models as well as in clinical conditions. Since traumatic brain injury is one of the strongest determinants of epileptogenesis, the present study focuses on the question whether a moderate long-term physical training can decrease susceptibility to seizures evoked following brain damage. Wistar rats received a mechanical brain injury and were subjected to daily running sessions on a treadmill for 21 days.

Inflammation induced at different developmental stages affects differently the range of microglial reactivity and the course of seizures evoked in the adult rat.

Background: In the brain, inflammation occurs following a variety of types of brain damage, including epileptic seizures. Proinflammatory cytokines, like IL-1β or TNFα, can increase neuronal excitability and initiate spontaneous seizures or epileptogenesis. Recent studies indicate that the effects can be attenuated or even abolished in animals subjected to inflammation-inducing treatments at earlier developmental stages, termed "preconditioning".