Seizures are more common early in life than in adulthood.
Bidirectional interactions between seizures and normal
developmental processes define their expression and outcomes.
Several developmentally regulated factors control neuronal
excitability. GABAA receptors hold a central role as they control
neuronal activity in an age-specific manner. Early in development,
GABAA receptors have depolarizing effects, which contribute to the
increased susceptibility of immature neurons to seizures but they
are also essential for normal brain development. During
development, there is a gradual shift to the "adult-type"
hyperpolarizing GABAA receptor signaling, creating more efficient
inhibition. Seizures may disrupt GABAA receptor signaling by
changing the expression of their subunits and by changing the
direction of GABAA responses, which, in certain situations, may be
detrimental for brain development. Furthermore, subcortical nuclei,
such as the substantia nigra, control the expression and
propagation of seizures in an age- and sex-dependent manner. These
endogenous control centers and signaling pathways are further
modified by independent genetic epigenetic, biologic, or other
factors, which further increase the heterogeneity in presentation
of seizures, their treatment, and their comorbidities. Elucidation
of these complex interactions and identification of biomarkers
guiding therapeutic interventions will be necessary to improve our
ability to treat early-life epilepsies.
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