Empirical comparison of the MEG and EEG: Animal models of the direct cortical response and epileptiform activity in neocortex

1991 ◽  
Vol 4 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Daniel S. Barth



1982 ◽  
Vol 14 (1) ◽  
pp. 63-70
Author(s):  
A. I. Roitbak ◽  
V. V. Fanardzhyan ◽  
D. S. Melkonyan ◽  
A. A. Melkonyan


1963 ◽  
Vol 15 (5) ◽  
pp. 882-888 ◽  
Author(s):  
Paul E. Stohr ◽  
Sidney Goldring ◽  
James L. O'Leary


1961 ◽  
Vol 11 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Yoshihiko IWASE ◽  
Takashi UCHIDA ◽  
Junzo OCHI


1984 ◽  
Vol 15 (3) ◽  
pp. 234-240
Author(s):  
V. M. Okudzhava ◽  
I. A. Mzhaviya ◽  
V. G. Goff


2002 ◽  
Vol 87 (5) ◽  
pp. 2471-2479 ◽  
Author(s):  
Lisa A. Gabel ◽  
Joseph J. LoTurco

Cortical dysplasias are associated with both epilepsy and cognitive impairments in humans. Similarly, several animal models of cortical dysplasia show that dysplasia causes increased seizure susceptibility and behavioral deficits in vivo and increased levels of excitability in vitro. As most current animal models involve either global disruptions in cortical architecture or the induction of lesions, it is not yet clear whether small spontaneous neocortical malformations are also associated with increased excitability or seizure susceptibility. Small groups of displaced neurons in layer I of the neocortex, ectopias, have been identified in patients with cognitive impairments, and similar malformations occur sporadically in some inbred lines of mice where they are associated with behavioral and sensory-processing deficits. In a previous study, we characterized the physiology of cells within neocortical ectopias, in one of the inbred lines (NXSM-D/Ei) and showed that the presence of multiple ectopias is associated with the generation of spontaneous epileptiform activity in slices. In this study, we use extracellular recordings from brain slices to show that even single-layer I ectopias are associated with higher excitability. Specifically, slices that contain single ectopias display epileptiform activity at significantly lower concentrations of the GABAA receptor antagonist bicuculline than do slices without ectopias (either from opposite hemispheres or animals without ectopias). Moreover, because removal of ectopias from slices does not restore normal excitability, enhanced excitability is not generated within the ectopia. Finally, we show that in vivo, mice with ectopias are more sensitive to the convulsant pentylenetetrazole than are mice without ectopias. Together these results suggest that alterations in cortical hemispheres containing focal layer I malformations increase cortical excitability and that even moderately small spontaneous cortical dysplasias are associated with increased excitability in vitro and in vivo.



Author(s):  
Fumiyuki Momma ◽  
H. Ian Sabin ◽  
Neil M. Branston ◽  
Lindsay Symon


1969 ◽  
Vol 3 (3) ◽  
pp. 91-98
Author(s):  
N. N. Zislina ◽  
N. A. Arkhipova


1971 ◽  
Vol 2 (1) ◽  
pp. 40-45
Author(s):  
M. M. Khananashvili ◽  
M. M. Bogoslovskii ◽  
�. G. Zarkeshev


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