Functional alterations in GABAergic fast-spiking interneurons in chronically injured epileptogenic neocortex

摘要: Progress toward developing effective prophylaxis and treatment of posttraumatic epilepsy depends on a detailed understanding the basic underlying mechanisms. One important factor contributing to epileptogenesis is decreased efficacy GABAergic inhibition. Here we tested hypothesis that output neocortical fast-spiking (FS) interneurons onto postsynaptic targets would be in undercut (UC) model chronic epileptogenesis. Using dual whole-cell recordings layer IV barrel cortex, found marked increase failure rate very large reduction amplitude unitary inhibitory currents (uIPSCs) from FS cells excitatory regular spiking (RS) neurons neighboring cells. Assessment paired pulse ratio presumed quantal release showed there was significant, but relatively modest, decrease synaptic probability non-significant size. A reduced density boutons axons biocytin-filled UC cells, together with higher coefficient variation uIPSC RS suggested number functional synapses presynaptically formed by may reduced. Given strength, other defects presynaptic vesicle machinery likely occur, as well.