Prenatal alcohol exposure affects developmental differentiation of interictal discharges in septal and temporal hippocampus.

Prenatal alcohol exposure (PAE) provokes lifelong CNS dysfunction, including an increased susceptibility to seizure disorders. We investigated hippocampal excitability in vitro in the offspring of dams exposed to a mild ethanol concentration throughout pregnancy (ethanol 15%v/v in drinking water). Hippocampal slices were prepared from the offspring at a young (Y, 21-30 postnatal days, PND) or adult (A, 60 PND) age, with controls from same age normal rats (N). Synchronous spontaneous interictal-type epileptiform discharges (IEDs) were induced by bathing the slices in Mg²⁺-free ACSF or in 4-Aminopyridine (4-AP, 50µΜ) and were recorded from CA1 pyramidal layer of temporal (T) and septal slices (S). Hippocampal slices readily generated IEDs following NMDA receptor activation or K⁺ conductance block, with frequency and duration depending on location (septal or temporal), age, the activating mechanism, and prior conditioning (N or PAE). From the two media, 4-AP induced higher frequency (always), shorter duration (mostly) IEDs compared to Mg ²⁺-free ACSF. Temporal IED frequency increased with age, whereas septal was stable, indicating an earlier maturation of the latter part. The hippocampal "T to S" (high to low) excitability gradient appeared at/later than the end of the first postnatal month and mostly concerned discharge frequency. Discharge duration generally decreased with maturation but appeared to depend on many factors, including conditioning. Prenatal alcohol exposure differentiated the control of synchronous discharges by NMDA receptors and K⁺ conductances, and their developmental evolution, thus suggesting potential mechanisms for aberrant hippocampal neuronal network function.