Alteration of synaptic plasticity by neonatal seizures in rat somatosensory cortex

Abstract

Seizures in newborns are associated with a high risk for subsequent epilepsy and adverse neurodevelopmental consequences. Understanding the mechanisms by which neonatal seizures adversely disturb the immature brain is important in developing therapeutic strategies. Using the convulsant agent flurothyl to mimic repetitive neonatal seizures we show that early-life seizures result in long-term alteration in the maintenance phase of long-term potentiation (LTP) in layer IV to layer II/III synapses of the somatosensory cortex without alteration of basal synaptic transmission, the induction phase of LTP and short-term depression. Such alterations may have a role in functional deficits seen following neonatal seizures.

Keywords: Early seizures; FP; GABA; LII/III; LIV; LTP; N-methyl-d-aspartate; NMDA; P; Plasticity; Somatosensory cortex; field potential; gamma-aminobutyric acid; layer 2/3; layer 4; long-term potentiation; postnatal day.