Epileptogenesis Following Neocortical Trauma from Two Sources of Disinhibition. Lie Yang and Larry S. Benardo. Departments of Pharmacology and Neurology, State University of New York, Health Science Center, Brooklyn, NY 11203.
APStracts 4:158N, 1997.
ABSTRACT
Intracellular and field potential recordings were obtained from superficial and deep neurons from both intact coronal rat somatosensory slices, and slices which had been acutely divided into a superficial strip of cortex (ÿ7E450 m from the pia) and a deep segment. Membrane properties for cells in the traumatized slices were similar to those of their counterparts in intact slices. However, synaptic hyperexcitability developed in the deep segments in which a majority of cells likely underwent dendrotomy. This hyperexcitability was manifested by epileptiform activity in 54% of traumatized slices. Measurements of fast GABAergic inhibitory strength showed these slices were disinhibited. Superficial delivery of tetrodotoxin to the upper 450 m of intact slices led to disinhibition of fast GABAergic transmission as well as an attendant increase in excitatory postsynaptic potential strength, but not epileptogenesis. Pharmacological maneuvers aimed at preventing glutamate- triggered increases in intracellular calcium (glutamate ionotropic antagonists, dantrolene, and BAPTA-AM) showed that a one hour treatment in these agents conferred protection against epileptogenesis. These results demonstrate that the seizure-like activity developing in deep dendrotomized cortical segments resulted from two sources of GABAergic disinhibition: the physical removal of important superficial inhibitory circuits and glutamate- triggered increases in intracellular calcium. 

Received 24 April 1997; accepted in final form 21 July 1997.
APS Manuscript Number J327-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 28 August 1997