Bicuculline-induced epileptogenesis in the human neocortex maintained in vitro.

摘要: Intracellular and extracellular recordings were made from human neocortical slices of the temporal lobe maintained in vitro. The treated with bicuculline methiodide to reduce synaptic inhibition mediated by tha gamma-aminobutyric acid A (GABAA) receptor. Spontaneously occurring epileptiform activity was never observed over 60 examined. All discharges elicited single-shock stimuli delivered underlying white matter or within cortical layers. Intracellularly, stimulus-induced discharge resembled paroxysmal depolarization shift (PDS). This potential neurons located between 200 2200 microns pia. It characterized a 100-1800 ms long which triggered burst firing action potentials, at times followed an afterdischarge. Simultaneous intracellular showed that each PDS reflected synchronous neuronal aggregate. voltage behaviour its preceding EPSP analyzed cells injected lidocaine derivative QX-314. amplitudes depolarizing envelope measured peak during falling phase both behaved as monotonic function membrane increasing amplitude hyperpolarization. In addition, much greater rate increase than early amplitude, thus suggesting conductance greater. Perfusion N-Methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-phosphonovaleric (APV) reduced duration field dose related fashion. effects APV intracellularly attenuation PDS's late blockade Similar findings also obtained using NMDA 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid. These data indicate reduction GABAA is sufficient elicit neocortex Mechanisms dependent upon contribute this type response mainly prolonging associated firing.